Journal articles on the topic 'CSCs markers'
To see the other types of publications on this topic, follow the link: CSCs markers.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'CSCs markers.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Jaggupilli, Appalaraju, and Eyad Elkord. "Significance of CD44 and CD24 as Cancer Stem Cell Markers: An Enduring Ambiguity." Clinical and Developmental Immunology 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/708036.
Full textAbstract:
Cancer stem cell population is a subset of cells capable of dictating invasion, metastasis, heterogeneity, and therapeutic resistance in tumours. Eradication of this rare population is a new insight in cancer treatment. However, prospective identification, characterization, and isolation of these CSCs have been a major challenge. Many studies were performed on surface markers for potential identification and isolation of CSCs. Lack of universal expression of surface markers limits their usage and no best combination of markers has yet been confirmed to identify CSCs capable of initiating and metastasizing tumours. CD44, a hyaluronic acid receptor, is one of the most commonly studied surface markers, which is expressed by almost every tumour cell. CD24, a heat stable antigen, is another surface marker expressed in many tumour types. However, their expression and prognostic value in isolating CSCs are still an enduring ambiguity. In this critical review, we assess the role of CD44 and CD24 in tumour initiation, development, and metastasis. We mainly focus on analysing the significance of CD44 and CD24 as CSC surface markers in combination or with other putative markers in different types of cancer.
2
Lan, Linxiang, and Axel Behrens. "Are There Specific Cancer Stem Cell Markers?" Cancer Research 83, no. 2 (January 18, 2023): 170–72. http://dx.doi.org/10.1158/0008-5472.can-22-2053.
Full textAbstract:
Abstract The cancer stem cell (CSC) model states that heterogeneous tumor cell populations are organized in a hierarchical manner, with a small population of CSCs at the apex. These CSCs are capable of self-renewal and giving rise to other cancer cell populations, conceptually analogous to the function of normal adult stem cells present in almost all organs. However, there has been significant controversy regarding the existence and identification of CSCs. We argue that technical differences in experimentation and CSC assays, CSC niche-dependency and plasticity, and CSC heterogeneity itself may explain some of the differences observed.
3
Hassan, Ghmkin, Said M. Afify, Neha Nair, Kazuki Kumon, Amira Osman, Juan Du, Hager Mansour, et al. "Hematopoietic Cells Derived from Cancer Stem Cells Generated from Mouse Induced Pluripotent Stem Cells." Cancers 12, no. 1 (December 29, 2019): 82. http://dx.doi.org/10.3390/cancers12010082.
Full textAbstract:
Cancer stem cells (CSCs) represent the subpopulation of cancer cells with the ability to differentiate into other cell phenotypes and initiated tumorigenesis. Previously, we reported generating CSCs from mouse induced pluripotent stem cells (miPSCs). Here, we investigated the ability of the CSCs to differentiate into hematopoietic cells. First, the primary cells were isolated from malignant tumors that were formed by the CSCs. Non-adherent cells (NACs) that arose from adherent cells were collected and their viability, as well as the morphology and expression of hematopoietic cell markers, were analyzed. Moreover, NACs were injected into the tail vein of busulfan conditioned Balb/c nude mice. Finally, CSCs were induced to differentiate to macrophages while using IL3 and SCF. The round nucleated NACs were found to be viable, positive for hematopoietic lineage markers and CD34, and expressed hematopoietic markers, just like homing to the bone marrow. When NACs were injected into mice, Wright–Giemsa staining showed that the number of white blood cells got higher than those in the control mice after four weeks. CSCs also showed the ability to differentiate toward macrophages. CSCs were demonstrated to have the potential to provide progenies with hematopoietic markers, morphology, and homing ability to the bone marrow, which could give new insight into the tumor microenvironment according to the plasticity of CSCs.
4
Hassn Mesrati, Malak, Amir Barzegar Behrooz, Asmaa Y. Abuhamad, and Amir Syahir. "Understanding Glioblastoma Biomarkers: Knocking a Mountain with a Hammer." Cells 9, no. 5 (May 16, 2020): 1236. http://dx.doi.org/10.3390/cells9051236.
Full textAbstract:
Gliomas are the most frequent and deadly form of human primary brain tumors. Among them, the most common and aggressive type is the high-grade glioblastoma multiforme (GBM), which rapidly grows and renders patients a very poor prognosis. Meanwhile, cancer stem cells (CSCs) have been determined in gliomas and play vital roles in driving tumor growth due to their competency in self-renewal and proliferation. Studies of gliomas have recognized CSCs via specific markers. This review comprehensively examines the current knowledge of the most significant CSCs markers in gliomas in general and in glioblastoma in particular and specifically focuses on their outlook and importance in gliomas CSCs research. We suggest that CSCs should be the superior therapeutic approach by directly targeting the markers. In addition, we highlight the association of these markers with each other in relation to their cascading pathways, and interactions with functional miRNAs, providing the role of the networks axes in glioblastoma signaling pathways.
5
Lee-Theilen, Mieun, Julia R. Hadhoud, Giulietta Volante, Delaine D. Fadini, Julia Eichhorn, Udo Rolle, and Henning C. Fiegel. "Co-Expression of CD34, CD90, OV-6 and Cell-Surface Vimentin Defines Cancer Stem Cells of Hepatoblastoma, Which Are Affected by Hsp90 Inhibitor 17-AAG." Cells 10, no. 10 (September 29, 2021): 2598. http://dx.doi.org/10.3390/cells10102598.
Full textAbstract:
Cancer stem cells (CSCs) are nowadays one of the major focuses in tumor research since this subpopulation was revealed to be a great obstacle for successful treatment. The identification of CSCs in pediatric solid tumors harbors major challenges because of the immature character of these tumors. Here, we present CD34, CD90, OV-6 and cell-surface vimentin (csVimentin) as reliable markers to identify CSCs in hepatoblastoma cell lines. We were able to identify CSC characteristics for the subset of CD34+CD90+OV-6+csVimentin+-co-expressing cells, such as pluripotency, self-renewal, increased expression of EMT markers and migration. Treatment with Cisplatin as the standard chemotherapeutic drug in hepatoblastoma therapy further revealed the chemo-resistance of this subset, which is a main characteristic of CSCs. When we treated the cells with the Hsp90 inhibitor 17-AAG, we observed a significant reduction in the CSC subset. With our study, we identified CSCs of hepatoblastoma using CD34, CD90, OV-6 and csVimentin. This set of markers could be helpful to estimate the success of novel therapeutic approaches, as resistant CSCs are responsible for tumor relapses.
6
Lee, Shiao-Pieng, Pei-Ling Hsieh, Chih-Yuan Fang, Pei-Ming Chu, Yi-Wen Liao, Chuan-Hang Yu, Cheng-Chia Yu, and Lo-Lin Tsai. "LINC00963 Promotes Cancer Stemness, Metastasis, and Drug Resistance in Head and Neck Carcinomas via ABCB5 Regulation." Cancers 12, no. 5 (April 26, 2020): 1073. http://dx.doi.org/10.3390/cancers12051073.
Full textAbstract:
Accumulating studies have indicated that long non-coding RNAs (lncRNAs) participate in the regulation of cancer stem cells (CSCs), which are crucial in tumor initiation, metastasis, relapse, and therapy resistance. In the current study, RT-PCR analysis was employed to evaluate the expression of LINC00963 in tumor tissues and oral CSCs. Stemness phenotypes and the expression of CSCs markers in oral cancer cells transfected with sh-LINC00963 were examined. Our results showed that the expression of the lncRNA LINC00963 was up-regulated in oral cancer tissues and CSCs. We found that the downregulation of LINC00963 inhibited CSC hallmarks, such as migration, invasion and colony formation capacity. Moreover, suppression of LINC00963 reduced the activity of stemness marker ALDH1, the percentage of self-renewal, chemoresistance and the expression of multidrug-resistance transporter ABCB5. Most importantly, we demonstrated that knockdown of LINC00963 decreased self-renewal, invasion and colony formation ability via ABCB5. Analysis of TCGA (the Cancer Genome Atlas) datasets suggested that the level of LINC00963 was positively correlated with the expression of the cancer stemness markers (Sox2 and CD44) and drug resistance markers (ABCG2 and ABCB5). Altogether, our results showed that suppression of LINC00963 may be beneficial to inhibit chemoresistance and cancer relapse in oral cancer patients.
7
Harris, Koran S., and Bethany A. Kerr. "Prostate Cancer Stem Cell Markers Drive Progression, Therapeutic Resistance, and Bone Metastasis." Stem Cells International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/8629234.
Full textAbstract:
Metastatic or recurrent tumors are the primary cause of cancer-related death. For prostate cancer, patients diagnosed with local disease have a 99% 5-year survival rate; however, this 5-year survival rate drops to 28% in patients with metastatic disease. This dramatic decline in survival has driven interest in discovering new markers able to identify tumors likely to recur and in developing new methods to prevent metastases from occurring. Biomarker discovery for aggressive tumor cells includes attempts to identify cancer stem cells (CSCs). CSCs are defined as tumor cells capable of self-renewal and regenerating the entire tumor heterogeneity. Thus, it is hypothesized that CSCs may drive primary tumor aggressiveness, metastatic colonization, and therapeutic relapse. The ability to identify these cells in the primary tumor or circulation would provide prognostic information capable of driving prostate cancer treatment decisions. Further, the ability to target these CSCs could prevent tumor metastasis and relapse after therapy allowing for prostate cancer to finally be cured. Here, we will review potential CSC markers and highlight evidence that describes how cells expressing each marker may drive prostate cancer progression, metastatic colonization and growth, tumor recurrence, and resistance to treatment.
8
Gu, Yuanzhuo, Xin Zheng, and Junfang Ji. "Liver cancer stem cells as a hierarchical society: yes or no?" Acta Biochimica et Biophysica Sinica 52, no. 7 (June 3, 2020): 723–35. http://dx.doi.org/10.1093/abbs/gmaa050.
Full textAbstract:
Abstract Cancer stem cells (CSCs) are cells possessing abilities of self-renewal, differentiation, and tumorigenicity in NOD/SCID mice. Based on this definition, multiple cell surface markers (such as CD24, CD133, CD90, and EpCAM) as well as chemical methods are discovered to enrich liver CSCs in the recent decade. Accumulated studies have revealed molecular signatures and signaling pathways involved in regulating different liver CSCs. Among liver CSCs positive for different markers, some molecular features and regulatory pathways are commonly shared, while some are only unique in certain CSC populations. These studies imply that liver CSCs exhibit diverse heterogeneity, while a functional relationship also exists. The aim of this review is to revisit the society of liver CSCs and summarize the common or unique molecular features of known liver CSCs. We hope to call for attention of researchers on the relationship of the liver CSC subgroups and to provide clues on the hierarchical structure of the liver CSC society.
9
Daya, Hiba Abou, Sana Kouba, Hakim Ouled-Haddou, Nazim Benzerdjeb, Marie-Sophie Telliez, Charles Dayen, Henri Sevestre, Loïc Garçon, Frédéric Hague, and Halima Ouadid-Ahidouch. "Orai3-Mediates Cisplatin-Resistance in Non-Small Cell Lung Cancer Cells by Enriching Cancer Stem Cell Population through PI3K/AKT Pathway." Cancers 13, no. 10 (May 12, 2021): 2314. http://dx.doi.org/10.3390/cancers13102314.
Full textAbstract:
The development of the resistance to platinum salts is a major obstacle in the treatment of non-small cell lung cancer (NSCLC). Among the reasons underlying this resistance is the enrichment of cancer stem cells (CSCs) populations. Several studies have reported the involvement of calcium channels in chemoresistance. The Orai3 channel is overexpressed and constitutes a predictive marker of metastasis in NSCLC tumors. Here, we investigated its role in CSCs populations induced by Cisplatin (CDDP) in two NSCLC cell lines. We found that CDDP treatment increased Orai3 expression, but not Orai1 or STIM1 expression, as well as an enhancement of CSCs markers. Moreover, Orai3 silencing or the reduction of extracellular calcium concentration sensitized the cells to CDDP and led to a reduction in the expression of Nanog and SOX-2. Orai3 contributed to SOCE (Store-operated Calcium entry) in both CDDP-treated and CD133+ subpopulation cells that overexpress Nanog and SOX-2. Interestingly, the ectopic overexpression of Orai3, in the two NSCLC cell lines, lead to an increase of SOCE and expression of CSCs markers. Furthermore, CD133+ cells were unable to overexpress neither Nanog nor SOX-2 when incubated with PI3K inhibitor. Finally, Orai3 silencing reduced Akt phosphorylation. Our work reveals a link between Orai3, CSCs and resistance to CDDP in NSCLC cells.
10
Alcalá, Sonia, Paola Martinelli, Patrick C. Hermann, Christopher Heeschen, and Bruno Sainz. "The Anthrax Toxin Receptor 1 (ANTXR1) Is Enriched in Pancreatic Cancer Stem Cells Derived from Primary Tumor Cultures." Stem Cells International 2019 (May 2, 2019): 1–13. http://dx.doi.org/10.1155/2019/1378639.
Full textAbstract:
Pancreatic ductal adenocarcinoma (PDAC) is currently the fourth leading cause of cancer-related mortality. Cancer stem cells (CSCs) have been shown to be the drivers of pancreatic tumor growth, metastasis, and chemoresistance, but our understanding of these cells is still limited by our inability to efficiently identify and isolate them. While a number of markers capable of identifying pancreatic CSCs (PaCSCs) have been discovered since 2007, there is no doubt that more markers are still needed. The anthrax toxin receptor 1 (ANTXR1) was identified as a functional biomarker of triple-negative breast CSCs, and PDAC patients stratified based on ANTXR1 expression levels showed increased mortality and enrichment of pathways known to be necessary for CSC biology, including TGF-β, NOTCH, Wnt/β-catenin, and IL-6/JAK/STAT3 signaling and epithelial to mesenchymal transition, suggesting that ANTXR1 may represent a putative PaCSC marker. In this study, we show that ANTXR1+ cells are not only detectable across a panel of 7 PDAC patient-derived xenograft primary cultures but ANTXR1 expression significantly increased in CSC-enriched 3D sphere cultures. Importantly, ANTXR1+ cells also coexpressed other known PaCSC markers such as CD44, CD133, and autofluorescence, and ANTXR1+ cells displayed enhanced CSC functional and molecular properties, including increased self-renewal and expression of pluripotency-associated genes, compared to ANTXR1- cells. Thus, this study validates ANTXR1 as a new PaCSC marker and we propose its use in identifying CSCs in this tumor type and its exploitation in the development of CSC-targeted therapies for PDAC.
11
Weaver, David T., Irina M. Shapiro, Alan G. Derr, Daniel Paterson, and Jonathan A. Pachter. "Use of gene expression and alternative splicing signatures to discriminate breast cancer stem cells from fibroblasts." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): 1057. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.1057.
Full textAbstract:
1057 Background: Tumors frequently contain cancer stem cells (CSCs) or tumor-initiating subpopulations, with an ability to self-renew and regenerate all cell types within the tumor. Basal-like breast cancers exhibit features of CSCs, including expression of surface markers, even though these cells are rare. Given the role of CSCs in the recurrence and spread of cancer, there is an urgent need to develop new therapeutic agents that target CSCs. Development of CSC-targeted drugs will be greatly facilitated by biomarkers that can identify CSCs to aid in patient selection and determination of drug response. Defining the CSCs in tumors is complicated by the high mesenchymal nature of fibroblasts. Analysis of gene expression and alternative splicing patterns in CSCs that are not observed in fibroblasts may provide valuable new CSC-specific markers. Methods: Alternative splicing and gene expression microarray strategies were used to identify selected exons and differentially expressed genes between 10 Basal human breast cancer cell lines and a combination of 12 Luminal and 3 fibroblast cell lines. Q-PCR analysis was conducted to determine candidate CSC gene differential expression between Basal, Luminal, and Fibroblast cells lines. Results: Expression levels of 11 genes were higher and 24 genes were lower in the Basal cell lines versus Luminal or fibroblastic cell lines. Comparison of Basal cell lines to the Luminal/Fibroblast cell lines identified 36 cassette exons that were included, and 26 that were excluded in Basal cell lines. Also, 19 genes were upregulated in Basal cell lines compared to the other groups as detected by Q-PCR. Interestingly, the 19-multigene model defined the Triple Negative Breast Cancer patients that were Likely to Recur under standard chemotherapy with a p = 1.90e-03 and AUC 0.723. Conclusions: Gene and exon marker sets distinguish CSC versus fibroblasts and may be instructive in identifying patients that recur early in Triple Negative Breast Cancer. The CSC-associated RNA signatures identified here will be further refined to develop new CSC-specific diagnostic markers to stratify breast cancer patients and monitor response to novel CSC-targeted therapies.
12
Wu, Hsing-Ju, and Pei-Yi Chu. "Role of Cancer Stem Cells in Cholangiocarcinoma and Therapeutic Implications." International Journal of Molecular Sciences 20, no. 17 (August 25, 2019): 4154. http://dx.doi.org/10.3390/ijms20174154.
Full textAbstract:
Cholangiocarcinoma (CCA) is the second most common type of liver cancer, and is highly aggressive with very poor prognosis. CCA is classified into intrahepatic cholangiocarcinoma (iCCA) and extra-hepatic cholangiocarcinoma (eCCA), which is further stratified into perihilar (pCCA) and distal (dCCA). Cancer stem cells (CSCs) are a subpopulation of cancer cells capable of tumor initiation and malignant growth, and are also responsible for chemoresistance. Thus, CSCs play an important role in CCA carcinogenesis. Surface markers such as CD133, CD24, CD44, EpCAM, Sox2, CD49f, and CD117 are important for identifying and isolating CCA CSCs. CSCs are present in the tumor microenvironment (TME), termed ‘CSC niche’, where cellular components and soluble factors interact to promote tumor initiation. Epithelial-to-mesenchymal transition (EMT) is another important mechanism underlying carcinogenesis, involved in the invasiveness, metastasis and chemoresistance of cancer. It has been demonstrated that EMT plays a critical role in generating CSCs. Therapies targeting the surface markers and signaling pathways of CCA CSCs, proteins involved in TME, and immune checkpoint proteins are currently under investigation. Therefore, this review focuses on recent studies on the roles of CSCs in CCA; the possible therapeutic strategies targeting CSCs of CCA are also discussed.
13
Kumbar, Vijay M., Uday M. Muddapur, Kishore G. Bhat, Shwetha H.R., Manohar S. Kugaji, and Malleswara Rao Peram. "Indirect Immunofluorescence and Tumorspheres Enrichment Technique for Identifying Cancer Stem Cell Markers in Cancer Cell Lines From Primary Oral Cancer Tissues: An In Vitro Study." Journal of Advanced Oral Research 11, no. 2 (July 24, 2020): 224–30. http://dx.doi.org/10.1177/2320206820941379.
Full textAbstract:
Aim: The cancer stem cells (CSCs) are known to be responsible for drug resistance and cancer relapse in the treatment of cancer. Identification and isolation of CSCs and study of their properties will play a crucial role in developing an effective drug against these targets. The aim of the study was to isolate CSCs from primary cancer by the tumorspheres enrichment method, to confirm by indirect immunofluorescence and gene expression of stem cell markers by using real-time polymerase chain reaction (RT-PCR) technique. Materials and Methods: In this in vitro study, we enriched oral CSCs through tumorsphere formation assay from seven primary cultures of OSCC patients with defined serum media. The expression and localization of the cell surface markers of CD133 and CD44 were tested by indirect immunofluorescence. Gene expression of stem cell markers such as CD44, CD133, Oct4, Sox2, and Nanog were quantified by RT-PCR technique. One-way analysis of variance was applied to analyze gene expression. Results: Tumorsphere formation has been used to isolate the CSCs from the OSCC tissue culture. Both CD133 and CD44 antibody confirmed the presence of CSCs through indirect immunofluorescence. In comparison to parental cell lines, the expression levels of CD133, CD44, Oct4, Sox2, and Nanog stem cell were significantly higher in CSC-enriched subpopulations. Conclusions: The cost-effective spheroid enrichment and the indirect immunofluorescence methods are useful for the isolation of CSCs from the primary tumor.
14
Song, Jingwen, Yanrong Qian, Maria Evers, Corinne M. Nielsen, and Xiaozhuo Chen. "Cancer Stem Cell Formation Induced and Regulated by Extracellular ATP and Stanniocalcin-1 in Human Lung Cancer Cells and Tumors." International Journal of Molecular Sciences 23, no. 23 (November 25, 2022): 14770. http://dx.doi.org/10.3390/ijms232314770.
Full textAbstract:
Cancer stem cells (CSCs) are closely associated with metastasis and epithelial mesenchymal transition (EMT). We previously reported that extracellular ATP (eATP) induces and regulates EMT in cancer cells. We recently found that the gene stanniocalcin 1 (STC1) is significantly upregulated by eATP in human non-small lung cancer (NSCLC) A549 cells; however, the relationships among eATP, CSCs, and STC1 were largely unknown. In this study, we performed gene knockdown and knockout, and a wide variety of functional assays to determine if and how eATP and STC1 induce CSCs in NSCLC A549 and H1299 cells. Our data show that, in both cultured cells and tumors, eATP increased the number of CSCs in the cancer cell population and upregulated CSC-related genes and protein markers. STC1 deletion led to drastically slower cell and tumor growth, reduced intracellular ATP levels and CSC markers, and metabolically shifted STC1-deficient cells from an energetic state to a quiescent state. These findings indicate that eATP induces and regulates CSCs at transcriptional, translational, and metabolic levels, and these activities are mediated through STC1 via mitochondria-associated ATP synthesis. These novel findings offer insights into eATP-induced CSCs and identify new targets for inhibiting CSCs.
15
Munro, Matthew J., Susrutha K. Wickremesekera, Lifeng Peng, Swee T. Tan, and Tinte Itinteang. "Cancer stem cells in colorectal cancer: a review." Journal of Clinical Pathology 71, no. 2 (September 23, 2017): 110–16. http://dx.doi.org/10.1136/jclinpath-2017-204739.
Full textAbstract:
Colorectal cancer (CRC) is the second most common cancer in women and the third most common in men. Adenocarcinoma accounts for 90% of CRC cases. There has been accumulating evidence in support of the cancer stem cell (CSC) concept of cancer which proposes that CSCs are central in the initiation of cancer. CSCs have been the focus of study in a range of cancers, including CRC. This has led to the identification and understanding of genes involved in the induction and maintenance of pluripotency of stem cells, and markers for CSCs, including those investigated specifically in CRC. Knowledge of the expression pattern of CSCs in CRC has been increasing in recent years, revealing a heterogeneous population of cells within CRC ranging from pluripotent to differentiated cells, with overlapping and sometimes unique combinations of markers. This review summarises current literature on the understanding of CSCs in CRC, including evidence of the presence of CSC subpopulations, and the stem cell markers currently used to identify and localise these CSC subpopulations. Future research into this field may lead to improved methods for early detection of CRC, novel therapy and monitoring of treatment for CRC and other cancer types.
16
Shukla, Samriddhi, Sajid Khan, Sonam Sinha, and Syed Musthapa Meeran. "Lung Cancer Stem Cells: An Epigenetic Perspective." Current Cancer Drug Targets 18, no. 1 (December 8, 2017): 16–31. http://dx.doi.org/10.2174/1568009617666170206104623.
Full textAbstract:
Lung cancer remains the major cause of human mortality among all the cancer types despite the colossal amount of efforts to prevent the cancer onset and to provide the appropriate cure. Recent reports have identified that important contributors of lung cancer-related mortality are the drug resistance and aggressive tumor relapse, the characteristics contributed by the presence of lung cancer stem cells (CSCs). The identification of lung CSCs is inherently complex due to the quiescent nature of lung epithelium, which makes the distinction between the normal lung epithelium and lung CSCs difficult. Recently, multiple researches have helped in the identification of lung CSCs based on the presence or absence of certain specific types of stem cell markers. Maintenance of lung CSCs is chiefly mediated through the epigenetic modifications of their genome. In this review, we will discuss about the origin of lung CSCs and the role of epigenetic modifications in their maintenance. We will also discuss in brief the major lung CSC markers and the therapeutic approaches to selectively target this population of cells.
17
Lin, Kangyu, and John Paul Shen. "Abstract 6066: Elucidating cancer stem cells heterogeneity in colorectal cancer by single-cell RNA sequencing." Cancer Research 82, no. 12_Supplement (June 15, 2022): 6066. http://dx.doi.org/10.1158/1538-7445.am2022-6066.
Full textAbstract:
Abstract Cancer stem cells (CSCs) are a small subpopulation of cells with capabilities of self-renewal and differentiation potential and have been suggested to play a critical role in tumor-initiation, metastasis, and multidrug resistance. The marker genes used to identify CSCs in CRC and transcriptional state of these cell is not fully elucidated due to the plasticity and dynamic nature of CSCs. In this study, we perform single-cell RNA sequencing (scRNA-seq) on primary CRC and liver metastases from CRC to evaluate the CSC population. We profiled approximately 80,000 single cells from neoadjuvant chemotherapy (NAC) treated patients generated using 10X Chromium scRNA-seq and Illumina platforms. A total of 16 samples were analyzed (5 colon tumor, 3 colon matched normal, 3 liver metastasis, 5 liver matched normal), 4 samples failed quality control and were excluded. Following extensive quality control and batch effect correction, we performed dimensionality reduction and differential expression analysis with Seurat v3.0 and custom R packages. We used a set of 11 canonical colon CSC marker genes (CD44, PROM1, LGR5, LRIG1, ASCL2, EPHB2, OLFM4, AXIN2, SLC12A2, RNF43, LEFTY1) as CSCs signature to score the stemness of each cell by AddModuleScore. Established marker genes were used to identify cell type assignment including stem/TA, immature enterocytes, immature secretory, enterocytes, Best4 enterocytes, goblet, tuff, CD4, CD8, Treg, NK, B, plasma, macrophages, monocytes, dendritic cells, fibroblasts, endothelium, glia, pericytes and hepatocytes. In the 16,703 epithelial cells, the CSC signature genes were diffusely expressed in stem/TA and immature epithelium but not in a specific cell cluster. There was minimal overlap in expression of the 11 CSC marker genes at the single-cell level. By clustering the CSCs identified by high CSC signature score, we found CSCs grouped distinctly by patients, indicating significant patient to patient variability. Furthermore, CSCs did not cluster by positivity for any specific marker gene, suggesting that marker genes may just be markers, and do not define distinct transcriptional states. Gene set enrichment analysis (GSEA) showed intestinal stemness was significantly enriched (FDR < 0.01) in CSCs compared with non-CSCs. Comparing CSCs to stem cells from normal samples, suppression of the fatty acid metabolism pathway was the only common feature seen in CSCs from each tumor. The heterogeneity of CSC marker genes in CRC tumor cells suggests that defining CSCs by single or few marker genes is inadequate. GSEA verified that a CSC scoring system aggregating expression of 11 canonical colon CSC marker genes can identify CSCs from scRNA-seq. There is marked transcriptional heterogeneity in CSCs, with few common features from CSCs from different tumors. It is hoped that future study of how the diversity of CSCs states evolve under chemotherapy will shed light on overcoming chemo-resistance. Citation Format: Kangyu Lin, John Paul Shen. Elucidating cancer stem cells heterogeneity in colorectal cancer by single-cell RNA sequencing [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 6066.
18
Zhang, Xiaoming, Ke Meng, Yujie Pu, Chao Wang, Yingying Chen, and Linlin Wang. "Hyperglycemia Altered the Fate of Cardiac Stem Cells to Adipogenesis through Inhibiting the β-Catenin/TCF-4 Pathway." Cellular Physiology and Biochemistry 49, no. 6 (2018): 2254–63. http://dx.doi.org/10.1159/000493828.
Full textAbstract:
Background/Aims: Hyperglycemia is an important risk factor for the most severe cardiovascular diseases in patients with diabetes. It has been demonstrated that cardiac stem cells (CSCs) play a pivotal role in the maintenance of cardiac homeostasis and regeneration. However, the mechanism underlying the influence of diabetes on CSCs remains unclear. This study demonstrated that hyperglycemia might promote adipogenesis in CSCs, which induces a decline in myocardial regeneration capability in diabetes. Methods: CSCs were isolated and cultured in high-glucose medium. The levels of β-catenin and TCF-4 in CSCs were determined by immunofluorescence staining and western blot analysis. Adipogenic transcriptional factors and CSCs markers were also examined by flow cytometry and western blot analysis after adipogenesis induction. In addition, Oil Red O staining was performed to investigate lipid droplet formation during adipogenesis induction with or without LiCl, a potent activator of TCF/β-catenin-dependent transcription. Results: High-glucose conditions inhibited nuclear translocation of β-catenin/TCF-4 and promoted adipogenesis in CSCs. After adipogenesis induction, expression of adipogenic transcriptional factors (PPARγ, ADD1, and C/EBPα) were increased (P < 0.01) and that of CSCs markers (c-Kit, Sca-1, MDR-1, and isl-1) were decreased (P< 0.01) in CSCs in the high-glucose group. Furthermore, lipid droplet formation was increased in CSCs cultured with high glucose, while LiCl attenuated lipid droplet formation in these CSCs (P < 0.01). Conclusion: These results demonstrated that hyperglycemia inhibited the β-catenin/TCF-4 pathway and promoted CSCs adipogenesis. Our findings suggest a new opportunity for future interventional strategie for abnormal myocardial regeneration and epicardial fat in patients with diabetes.
19
Brescia, Paola, Cristina Richichi, and Giuliana Pelicci. "Current Strategies for Identification of Glioma Stem Cells: Adequate or Unsatisfactory?" Journal of Oncology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/376894.
Full textAbstract:
Cancer stem cells (CSCs) were isolated in multiple tumor types, including human glioblastomas, and although the presence of surface markers selectively expressed on CSCs can be used to isolate them, no marker/pattern of markers are sufficiently robust to definitively identify stem cells in tumors. Several markers were evaluated for their prognostic value with promising early results, however none of them was proven to be clinically useful in large-scale studies, leading to outstanding efforts to identify new markers. Given the heterogeneity of human glioblastomas further investigations are necessary to identify both cancer stem cell-specific markers and the molecular mechanisms sustaining the tumorigenic potential of these cells to develop tailored treatments. Markers for glioblastoma stem cells such as CD133, CD15, integrin-α6, L1CAM might be informative to identify these cells but cannot be conclusively linked to a stem cell phenotype. Overlap of expression, functional state and morphology of different subpopulations lead to carefully consider the techniques employed so far to isolate these cells. Due to a dearth of methods and markers reliably identifying the candidate cancer stem cells, the isolation/enrichment of cancer stem cells to be therapeutically targeted remains a major challenge.
20
Prayogo, Ami Ashariati, Andi Yasmin Wijaya, Winona May Hendrata, Steven Sheng Looi, Reny I’tishom, Lukman Hakim, Fedik Abdul Rantam, I. Ketut Sudiana, and Abdurachman Abdurachman. "Dedifferentiation of MCF-7 Breast Cancer Continuous Cell Line, Development of Breast Cancer Stem Cells (BCSCs) Enriched Culture and Biomarker Analysis." Indonesian Biomedical Journal 12, no. 2 (June 29, 2020): 115–23. http://dx.doi.org/10.18585/inabj.v12i2.977.
Full textAbstract:
BACKGROUND: Cancer stem cells (CSCs) eradication might serve as a robust approach for cancer eradication. MCF-7 as breast cancer continuous cell line is known to contain breast CSCs (BCSCs) for its capability to maintain its original tumor population. CSCs enriched culture is a fundamental tool for CSCs targeted therapy development. Effective and unsophisticated CSCs dedifferentiation protocol for producing CSCs enriched culture is needed.METHODS: MCF-7 cells were cultured initially in Dulbecco's Modified Eagle Medium (DMEM) low glucose medium then changed to DMEM:F12. Serum starvation was performed during each medium refreshment gradually with fetal bovine serum (FBS) concentration of 10%, 5%, 2.5% until reaching 1% FBS concentration. Stable MCF-7 culture was then adapted to serum free culture system, containing DMEM:F12, epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), and B27 supplement as dedifferentiation protocol for 18 days. Cluster of differentiation (CD)44 and CD24 double staining immunocytochemistry was performed to evaluate cell stemness.RESULTS: The population of cells expressing BCSCs markers (CD44+/CD24low) in non-adherent single cells subpopulation was significantly increased after the dedifferentiation procedure (70.39%) compared to control groups (0.71%) (p<0.05). In contrast, the expression of BCSCs marker in adherent single cells subpopulation and for both adherent and non-adherent mammosphere the BCSCs markers showed a stable expression.CONCLUSION: BCSCs enrichment of breast cancer cell cultures from MCF-7 breast cancer cell line can be performed. Breast cancer cell plasticity is observed during the dedifferentiation protocol. Development of dedifferentiation inducing protocols can serve as an important foundation for breast cancer therapy development through BCSCs elimination.KEYWORDS: breast neoplasms, cell line, dedifferentiation, immunohistochemistry, neoplastic stem cells
21
Oswald, James T., Haritosh Patel, Daid Khan, Ninweh N. Jeorje, Hossein Golzar, Erin L. Oswald, and Shirley Tang. "Drug Delivery Systems Using Surface Markers for Targeting Cancer Stem Cells." Current Pharmaceutical Design 26, no. 17 (June 7, 2020): 2057–71. http://dx.doi.org/10.2174/1381612826666200406084900.
Full textAbstract:
The innate abilities of cancer stem cells (CSCs), such as multi-drug resistance, drug efflux, quiescence and ionizing radiation tolerance, protect them from most traditional chemotherapeutics. As a result, this small subpopulation of persistent cells leads to more aggressive and chemoresistant cancers, causing tumour relapse and metastasis. This subpopulation is differentiated from the bulk tumour population through a wide variety of surface markers expressed on the cell surface. Recent developments in nanomedicine and targeting delivery methods have given rise to new possibilities for specifically targeting these markers and preferentially eliminating CSCs. Herein, we first summarize the range of surface markers identifying CSC populations in a variety of cancers; then, we discuss recent attempts to actively target CSCs and their niches using liposomal, nanoparticle, carbon nanotube and viral formulations.
22
Lee, Hwa-Yong, and In-Sun Hong. "Targeting Liver Cancer Stem Cells: An Alternative Therapeutic Approach for Liver Cancer." Cancers 12, no. 10 (September 24, 2020): 2746. http://dx.doi.org/10.3390/cancers12102746.
Full textAbstract:
The first report of cancer stem cell (CSC) from Bruce et al. has demonstrated the relatively rare population of stem-like cells in acute myeloid leukemia (AML). The discovery of leukemic CSCs prompted further identification of CSCs in multiple types of solid tumor. Recently, extensive research has attempted to identity CSCs in multiple types of solid tumors in the brain, colon, head and neck, liver, and lung. Based on these studies, we hypothesize that the initiation and progression of most malignant tumors rely largely on the CSC population. Recent studies indicated that stem cell-related markers or signaling pathways, such as aldehyde dehydrogenase (ALDH), CD133, epithelial cell adhesion molecule (EpCAM), Wnt/β-catenin signaling, and Notch signaling, contribute to the initiation and progression of various liver cancer types. Importantly, CSCs are markedly resistant to conventional therapeutic approaches and current targeted therapeutics. Therefore, it is believed that selectively targeting specific markers and/or signaling pathways of hepatic CSCs is an effective therapeutic strategy for treating chemotherapy-resistant liver cancer. Here, we provide an overview of the current knowledge on the hepatic CSC hypothesis and discuss the specific surface markers and critical signaling pathways involved in the development and maintenance of hepatic CSC subpopulations.
23
Elkashty, Osama A., Ghada Abu Elghanam, Xinyun Su, Younan Liu, Peter J. Chauvin, and Simon D. Tran. "Cancer stem cells enrichment with surface markers CD271 and CD44 in human head and neck squamous cell carcinomas." Carcinogenesis 41, no. 4 (November 19, 2019): 458–66. http://dx.doi.org/10.1093/carcin/bgz182.
Full textAbstract:
Abstract Head and neck squamous cell carcinoma (HNSCC) has a poor 5-year survival rate of 50%. One potential reason for treatment failure is the presence of cancer stem cells (CSCs). Several cell markers, particularly CD44, have been used to isolate CSCs. However, isolating a pure population of CSC in HNSCC still remains a challenging task. Recent findings show that normal oral stem cells were isolated using CD271 as a marker. Thus, we investigated the combined use of CD271 and CD44 to isolate an enriched subpopulation of CSCs, followed by their characterization in vitro, in vivo, and in patients’ tissue samples. Fluorescent-activated cell sorting was used to isolate CD44+/CD271+ and CD44+/CD271− from two human HNSCC cell lines. Cell growth and self-renewal were measured with MTT and sphere/colony formation assays. Treatment-resistance was tested against chemotherapy (cisplatin and 5-fluorouracil) and ionizing radiation. Self-renewal, resistance, and stemness-related genes expression were measured with qRT-PCR. In vivo tumorigenicity was tested with an orthotopic immunodeficient mouse model of oral cancer. Finally, we examined the co-localization of CD44+/CD271+ in patients’ tissue samples. We found that CD271+ cells were a subpopulation of CD44+ cells in human HNSCC cell lines and tissues. CD44+/CD271+ cells exhibited higher cell proliferation, sphere/colony formation, chemo- and radio-resistance, upregulation of CSCs-related genes, and in vivo tumorigenicity when compared to CD44+/CD271− or the parental cell line. These cell markers showed increased expression in patients with the increase of the tumor stage. In conclusion, using both CD44 and CD271 allowed the isolation of CSCs from HNSCC. These enriched CSCs will be more relevant in future treatment and HNSCC progression studies.
24
Badrinath, Narayanasamy, and So Yoo. "Recent Advances in Cancer Stem Cell-Targeted Immunotherapy." Cancers 11, no. 3 (March 5, 2019): 310. http://dx.doi.org/10.3390/cancers11030310.
Full textAbstract:
Cancer stem cells (CSCs) are one of the reasons for the relapse of cancer cells and metastasis. They have drug resistance against most chemotherapeutic agents. CSCs are also responsible for tumor cell heterogeneity and cause minimal residual disease. In order to achieve complete regression of tumors, CSCs have to be targeted. Recent advances in immunotherapies have shown promising outcomes in curing cancer, which are also applicable to target CSCs. CSCs express immune markers and exhibit specific immune characteristics in various cancers, which can be used in immunotherapies to target CSCs in the tumor microenvironment. Recently, various strategies have been used to target CSCs. Adaptive T-cells, dendritic cell (DC)-based vaccines, oncolytic viruses, immune checkpoint inhibitors, and combination therapies are now being used to target CSCs. Here, we discuss the feasibility of these immunological approaches and the recent trends in immunotherapies to target CSCs.
25
Tan, David, Imogen Roth, Agadha Wickremesekera, Paul Davis, Andrew Kaye, Theo Mantamadiotis, Stanley Stylli, and Swee Tan. "Therapeutic Targeting of Cancer Stem Cells in Human Glioblastoma by Manipulating the Renin-Angiotensin System." Cells 8, no. 11 (October 31, 2019): 1364. http://dx.doi.org/10.3390/cells8111364.
Full textAbstract:
Patients with glioblastoma (GB), a highly aggressive brain tumor, have a median survival of 14.6 months following neurosurgical resection and adjuvant chemoradiotherapy. Quiescent GB cancer stem cells (CSCs) invariably cause local recurrence. These GB CSCs can be identified by embryonic stem cell markers, express components of the renin-angiotensin system (RAS) and are associated with circulating CSCs. Despite the presence of circulating CSCs, GB patients rarely develop distant metastasis outside the central nervous system. This paper reviews the current literature on GB growth inhibition in relation to CSCs, circulating CSCs, the RAS and the novel therapeutic approach by repurposing drugs that target the RAS to improve overall symptom-free survival and maintain quality of life.
26
Afify, Said M., Ghmkin Hassan, Amira Osman, Anna Sanchez Calle, Hend M. Nawara, Maram Hussein Zahra, Samah EL-Ghlban, et al. "Metastasis of Cancer Stem Cells Developed in the Microenvironment of Hepatocellular Carcinoma." Bioengineering 6, no. 3 (August 23, 2019): 73. http://dx.doi.org/10.3390/bioengineering6030073.
Full textAbstract:
Metastasis develops when cancer cells spread from the primary site of a malignant tumor to the surrounding and distant tissues, and it is the most critical problem in cancer treatment. Our group developed cancer stem cells (CSCs) from induced pluripotent stem cells (iPSCs) in the presence of a conditioned medium (CM) of cancer-derived cells. The CSCs were characterized by the formation of malignant tumors in vivo, followed by metastasis. In this study, CSCs converted from mouse iPSCs in the presence of CM from hepatocellular carcinoma (HCC) cell line Huh7 cells. These converted cells (miPS-Huh7cm cells) were established as the metastatic cells. The generated CSCs were injected into the liver or spleen of nude mice. Almost one month after transplantation, the tumors were excised, and the primary cultured cells derived from the malignant tumors and metastatic nodules were evaluated by stemness and metastatic markers to compare their differences. The miPS-Huh7cm cells exhibited metastatic potential, and efficiently formed malignant tumors with lung and/or liver lesions in vivo, whereas the injected miPS formed teratoma. The primary cultured cells derived from the malignant tumors and metastatic nodules sustained the expression of stemness markers, such as Nanog, Klf4 and c-Myc, and acquired cancer stem markers, such as CD90, CD44 and ALDH1. Simultaneously, the expression of metastatic markers, such as Slug, Twist1 and vimentin, in primary cells derived from the malignant tumors, was higher than in metastatic nodules. The CSCs derived from iPSCs, forming malignant tumors and displaying high metastasis, will provide a good animal model to study the mechanisms of metastasis.
27
Cianciosi, Danila, Johura Ansary, Tamara Y. Forbes-Hernandez, Lucia Regolo, Denise Quinzi, Santos Gracia Villar, Eduardo Garcia Villena, et al. "The Molecular Basis of Different Approaches for the Study of Cancer Stem Cells and the Advantages and Disadvantages of a Three-Dimensional Culture." Molecules 26, no. 9 (April 29, 2021): 2615. http://dx.doi.org/10.3390/molecules26092615.
Full textAbstract:
Cancer stem cells (CSCs) are a rare tumor subpopulation with high differentiation, proliferative and tumorigenic potential compared to the remaining tumor population. CSCs were first discovered by Bonnet and Dick in 1997 in acute myeloid leukemia. The identification and isolation of these cells in this pioneering study were carried out through the flow cytometry, exploiting the presence of specific cell surface molecular markers (CD34+/CD38−). In the following years, different strategies and projects have been developed for the study of CSCs, which are basically divided into surface markers assays and functional assays; some of these techniques also allow working with a cellular model that better mimics the tumor architecture. The purpose of this mini review is to summarize and briefly describe all the current methods used for the identification, isolation and enrichment of CSCs, describing, where possible, the molecular basis, the advantages and disadvantages of each technique with a particular focus on those that offer a three-dimensional culture.
28
Herreros-Pomares, Alejandro. "Identification, Culture and Targeting of Cancer Stem Cells." Life 12, no. 2 (January 27, 2022): 184. http://dx.doi.org/10.3390/life12020184.
Full textAbstract:
Chemoresistance, tumor progression, and metastasis are features that are frequently seen in cancer that have been associated with cancer stem cells (CSCs). These cells are a promising target in the future of cancer therapy but remain largely unknown. Deregulation of pathways that govern stemness in non-tumorigenic stem cells (SCs), such as Notch, Wnt, and Hedgehog pathways, has been described in CSC pathogenesis, but it is necessary to conduct further studies to discover potential new therapeutic targets. In addition, some markers for the identification and characterization of CSCs have been suggested, but the search for specific CSC markers in many cancer types is still under development. In addition, methods for CSC cultivation are also under development, with great heterogeneity existing in the protocols used. This review focuses on the most recent aspects of the identification, characterization, cultivation, and targeting of human CSCs, highlighting the advances achieved in the clinical implementation of therapies targeting CSCs and remarking those potential areas where more research is still required.
29
Cadilho, Julio Cesar Ramos, Silvia Maria de Carvalho Lyra, Ana Beatriz Machado Lima, Carina Maciel da Silva Boghossian, and Cláudia Maria Pereira. "Stem cell markers expression evaluation in Oral Squamous Cell Carcinoma." Research, Society and Development 10, no. 13 (October 14, 2021): e314101320840. http://dx.doi.org/10.33448/rsd-v10i13.20840.
Full textAbstract:
Oral carcinogenesis is a highly complex process. Molecular studies demonstrate that some oral cancers progress from pre-neoplastic lesions. Cancer stem cells (CSCs), a small cellular group within the tumor, have currently received much attention by its self-renewal and tumor differentiation ability. It is considered that CSCs may be responsible for the relapse and metastasis of cancer. CSCs have been reported to express common embryonic stem cells markers such as Nestin and Nanog. The aim of the present study was to identify the presence of Nestin and Nanog markers in patients with oral squamous cell carcinoma (OSCC). Nine samples were collected from patients diagnosed with OSCC and two healthy oral mucosa were used as control. The markers expression in nine OSCC was determined by end-point PCR. The OSCC population analyzed was mostly composed of black and white males, with a mean age of 70.6 years, that reported alcohol and tobacco consumption. Nestin and Nanog stem cell markers were expressed in all OSCCs and normal samples analyzed. As these two markers have already been related to the mechanism of metastasis and relapses in cancer, its expression determination could help to understand the aggressive and invasive nature of OSCC.
30
McCartin, Conor, Candice Dussouillez, Chloé Bernhard, Eric Mathieu, Juliette Blumberger, Monique Dontenwill, Christel Herold-Mende, et al. "Polyethylenimine, an Autophagy-Inducing Platinum-Carbene-Based Drug Carrier with Potent Toxicity towards Glioblastoma Cancer Stem Cells." Cancers 14, no. 20 (October 15, 2022): 5057. http://dx.doi.org/10.3390/cancers14205057.
Full textAbstract:
The difficulty involved in the treatment of many tumours due to their recurrence and resistance to chemotherapy is tightly linked to the presence of cancer stem cells (CSCs). This CSC sub-population is distinct from the majority of cancer cells of the tumour bulk. Indeed, CSCs have increased mitochondrial mass that has been linked to increased sensitivity to mitochondrial targeting compounds. Thus, a platinum-based polyethylenimine (PEI) polymer–drug conjugate (PDC) was assessed as a potential anti-CSC therapeutic since it has previously displayed mitochondrial accumulation. Our results show that CSCs have increased specific sensitivity to the PEI carrier and to the PDC. The mechanism of cell death seems to be necrotic in nature, with an absence of apoptotic markers. Cell death is accompanied by the induction of a protective autophagy. The interference in the balance of this pathway, which is highly important for CSCs, may be responsible for a partial reversion of the stem-like phenotype observed with prolonged PEI and PDC treatment. Several markers also indicate the cell death mode to be capable of inducing an anti-cancer immune response. This study thus indicates the potential therapeutic perspectives of polycations against CSCs.
31
Yahaya, Badrul Hisham, Norashikin Zakaria, Noor Hanis Abu Halim, and Nazilah Satar. "ID:3004 Lung cancer stem cell and its therapeutic potential." Biomedical Research and Therapy 4, S (September 5, 2017): 15. http://dx.doi.org/10.15419/bmrat.v4is.221.
Full textAbstract:
Cancer stem cells (CSCs), a subpopulation of cancer cells with the ability to self-renew and giving rise to differentiated cancer cells, are thought to play a crucial role in tumour development, invasion, metastasis and recurrence. Treatments for lung cancer remain a challenging due to ineffectiveness of current available therapies to eradicate the quiescent and therapy-resistance of CSCs. Therefore, new treatment regime specifically targeting CSCs are needed to improve the effectiveness of lung cancer treatment. However the identification of lung CSCs especially in non-small cell lung cancer (NSCLC) remains challenging due to highly heterogeneous cell population and no standard markers to distinguish the lung CSCs from their cancer origins. The use of cell surface markers in isolation, identification and characterization of CSCs is one of the important tools as to understand the basic molecular composition and properties of CSCs and the pathways that of these heterogeneous population of cells are involved for future targeted therapy. Our group has identified, isolated and characterized putative lung CSCs from NSCLC cell line based on expression of combination CSCs markers, the CD166/CD44 and CD166/EpCAM using fluorescence activated cell sorting (FACS). The putative lung CSCs, the CD166+CD44+ CD166+EpCAM+ were characterized for multipotent and self-renewal capability using differentiation, clonogenic and spheroid assays. Following microarray gene expression study and bioinformatics analysis, our data has shown that the NF-κB was consistently expressed and shown to play a significant role in maintaining tumorigenicity of CSCs. In order to proof the role of NF-κB, the cells were treated with different concentrations of BMS-345541 (an inhibitor of NF-κB molecule) and the effectiveness of the treatments were evaluated through its ability to reduce self-renewal, expression of stemness genes (Sox2, Oct4, Klf4, Nanog and Sca-1), migration and epithelial to mesenchymal transition process (EMT) activities. The effectiveness of curcumin as drug sensitizer for effective therapy in treating chemoresistance of CSCs, was also investigated. The capability of CD166+/CD44+ and CD166+/EpCAM+ to differentiate into multipotent cell lineages (adipocytes and osteocyte), to form colony and to anchorage independent spheres and expressed stemness genes were shown in this study. The inhibition of NF-κB molecule using BMS-345441 has reduced the sphere forming capability, expression of stemness genes (Sox2, Nanog and Oct4), migration and expression of EMT genes in lung CSCs. Meanwhile, curcumin was found to reduce the cells proliferation activity and induced apoptosis of the cells. In addition, curcumin was also able to sensitize cisplatin, to supress the migration ability and inhibiting self-renewal capability of lung CSCs. Besides, the mRNA level of Sox2, Klf4, Nanog and Oct4 were down-regulated in lung CSCs after treatment with combination of both curcumin and cisplatin. Our findings suggest that NF-κB could be used as a potential targeted gene for lung cancer gene modification whereas curcumin could be used as potential natural compound that was able to sensitize the chemotherapy drug for effective cancer therapy.
32
Kobayashi, Natália Cristina Ciufa, and Samuel Marcos Ribeiro de Noronha. "Cancer stem cells: a new approach to tumor development." Revista da Associação Médica Brasileira 61, no. 1 (February 2015): 86–93. http://dx.doi.org/10.1590/1806-9282.61.01.086.
Full textAbstract:
Many theories have been proposed to explain the origins of cancer. Currently, evidences show that not every tumor cell is capable of initiating a tumor. Only a small part of the cancer cells, called cancer stem cells (CSCs), can generate a tumor identical to the original one, when removed from human tumors and transplanted into immunosuppressed mice. The name given to these cells comes from the resemblance to normal stem cells, except for the fact that their ability to divide is infinite. These cells are also affected by their microenvironment. Many of the signaling pathways, such as Wnt, Notch and Hedgehog, are altered in this tumoral subpopulation, which also contributes to abnormal proliferation. Researchers have found several markers for CSCs; however, much remains to be studied, or perhaps a universal marker does not even exist, since they vary among tumor types and even from patient to patient. It was also found that cancer stem cells are resistant to radiotherapy and chemotherapy. This may explain the re-emergence of the disease, since they are not completely eliminated and minimal amounts of CSCs can repopulate a tumor. Once the diagnosis in the early stages greatly increases the chances of curing cancer, identifying CSCs in tumors is a goal for the development of more effective treatments. The objective of this article is to discuss the origin of cancer according to the theory of stem cell cancer, as well as its markers and therapies used for treatment.
33
de Kluyver, Rachel, Jim Stauffer, Alan Brooks, Anil Shanker, and Tom Sayers. "Murine Hepatocellular Carcinoma Stem Cells Express Pluripotency-associated Transcription Factors and are Sensitive to Immune Mediated Apoptosis. (101.16)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 101.16. http://dx.doi.org/10.4049/jimmunol.184.supp.101.16.
Full textAbstract:
Abstract Current evidence supports the view that cancer stem cells (CSCs) constitute the primary pathogenic component of both metastases and minimal residual disease and that elimination of CSCs is required for cure. Cell surface markers have been used to identify CSCs but fail to identify CSC in all tumors from the same tissue or in all patients. Therefore there is a need to define and test more reliable markers of CSCs. Oct-4, Sox-2 and Nanog transcription factors are key regulatory factors in maintenance of pluripotency and have been demonstrated to be robust intracellular biomarkers for tissue and cancer stem cells. A GFP-based reporter driven by a promoter responsive to Nanog or Oct-4 was used to mark pluripotent tumor cells from in vitro cultured, cancer cell lines (breast cancer- 4T1.2), and from autochthonous hepatocellular carcinoma. The molecular profile of primary Akt/β-Cat-induced murine HCC recapitulates that observed in poor prognosis Ep-CAM+/AFP+ human HCC. Ep-CAM and CD133 and Nanog and Oct-4 are independent CSC markers. Directly ex vivo, murine HCC stem cells express abundant CD1d and MHC class II in addition to TNF-R2, lymphotoxin-β receptor (LTβR) and DR5. The functional significance of CD1d, MHC class II, TNF-R2, LTβR and DR5 expression will be assessed in future studies. This study will provide valuable proof-of-principle data to the merits of CSCs as targets for curative anti-cancer therapies.
34
Ibragimova, Marina, Matvey Tsyganov, and Nikolai Litviakov. "Tumour Stem Cells in Breast Cancer." International Journal of Molecular Sciences 23, no. 9 (May 2, 2022): 5058. http://dx.doi.org/10.3390/ijms23095058.
Full textAbstract:
Tumour stem cells (CSCs) are a self-renewing population that plays important roles in tumour initiation, recurrence, and metastasis. Although the medical literature is extensive, problems with CSC identification and cancer therapy remain. This review provides the main mechanisms of CSC action in breast cancer (BC): CSC markers and signalling pathways, heterogeneity, plasticity, and ecological behaviour. The dynamic heterogeneity of CSCs and the dynamic transitions of CSC− non-CSCs and their significance for metastasis are considered.
35
Koren, Ana, Matija Rijavec, Izidor Kern, Eva Sodja, Peter Korosec, and Tanja Cufer. "BMI1,ALDH1A1, andCD133Transcripts Connect Epithelial-Mesenchymal Transition to Cancer Stem Cells in Lung Carcinoma." Stem Cells International 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/9714315.
Full textAbstract:
Epithelial-mesenchymal transition (EMT) is the underlying mechanism of tumor invasion and metastasis. Evidences from lung cancer cellular models show EMT can trigger conversion to a cancer stem cell (CSC) phenotype. In this study, we assessed mRNA expression levels of EMT-inducing transcription factors (BMI1,TWIST1), CSC (CD133,ALDH1A1), and epithelial (EpCAM) markers in primary tumor and whole blood samples obtained from 57 patients with operable non-small-cell lung cancer (NSCLC) as well as in circulating tumor cells (CTCs) of 13 patients with metastatic disease; then possible associations between marker expressions were evaluated. In primary tumors as well as in whole blood, correlations betweenBMI1andALDH1A1and betweenBMI1andCD133mRNA expressions were identified. No correlations betweenTWIST1and CSC markers were observed.BMI1mRNA expression in tumors positively correlated withBMI1mRNA expression in blood. The immunohistochemical analysis confirmed coexpression of BMI1 and CSC markers in tumors. Gene expression profiling in CTCs revealed upregulated expression of EMT/CSC markers in CTCs. Our results suggest CSCs are present in both, tumor tissue and blood of NSCLC patients, whereas Bmi1 may play an important role in initiation and maintenance of CSCs and might be involved in the blood-borne dissemination of NSCLC.
36
Huang, Binjie, Xin Yan, and Yumin Li. "Cancer Stem Cell for Tumor Therapy." Cancers 13, no. 19 (September 26, 2021): 4814. http://dx.doi.org/10.3390/cancers13194814.
Full textAbstract:
Tumors pose a significant threat to human health. Although many methods, such as operations, chemotherapy and radiotherapy, have been proposed to eliminate tumor cells, the results are unsatisfactory. Targeting therapy has shown potential due to its specificity and efficiency. Meanwhile, it has been revealed that cancer stem cells (CSCs) play a crucial role in the genesis, development, metastasis and recurrence of tumors. Thus, it is feasible to inhibit tumors and improve prognosis via targeting CSCs. In this review, we provide a comprehensive understanding of the biological characteristics of CSCs, including mitotic pattern, metabolic phenotype, therapeutic resistance and related mechanisms. Finally, we summarize CSCs targeted strategies, including targeting CSCs surface markers, targeting CSCs related signal pathways, targeting CSC niches, targeting CSC metabolic pathways, inducing differentiation therapy and immunotherapy (tumor vaccine, CAR-T, oncolytic virus, targeting CSCs–immune cell crosstalk and immunity checkpoint inhibitor). We highlight the potential of immunity therapy and its combinational anti-CSC therapies, which are composed of different drugs working in different mechanisms.
37
Cheung, Sarah K. C., Po-Kai Chuang, Han-Wen Huang, Wendy W. Hwang-Verslues, Candy Hsin-Hua Cho, Wen-Bin Yang, Chia-Ning Shen, et al. "Stage-specific embryonic antigen-3 (SSEA-3) and β3GalT5 are cancer specific and significant markers for breast cancer stem cells." Proceedings of the National Academy of Sciences 113, no. 4 (December 17, 2015): 960–65. http://dx.doi.org/10.1073/pnas.1522602113.
Full textAbstract:
The discovery of cancer stem cells (CSCs), which are responsible for self-renewal and tumor growth in heterogeneous cancer tissues, has stimulated interests in developing new cancer therapies and early diagnosis. However, the markers currently used for isolation of CSCs are often not selective enough to enrich CSCs for the study of this special cell population. Here we show that the breast CSCs isolated with CD44+CD24-/loSSEA-3+ or ESAhiPROCRhiSSEA-3+ markers had higher tumorigenicity than those with conventional markers in vitro and in vivo. As few as 10 cells with CD44+CD24-/loSSEA-3+ formed tumor in mice, compared with more than 100 cells with CD44+CD24-/lo. Suppression of SSEA-3 expression by knockdown of the gene encoding β-1,3-galactosyltransferase 5 (β3GalT5) in the globo-series pathway, led to apoptosis in cancer cells specifically but had no effect on normal cells. This finding is further supported by the analysis of SSEA-3 and the two related globo-series epitopes SSEA4 and globo-H in stem cells (embryonic stem cells and induced pluripotent stem cells) and various normal and cancer cells, and by the antibody approach to target the globo-series glycans and the late-stage clinical trials of a breast cancer vaccine.
38
Pozzi, Valentina, Davide Sartini, Romina Rocchetti, Andrea Santarelli, Corrado Rubini, Stefano Morganti, Rachela Giuliante, et al. "Identification and Characterization of Cancer Stem Cells from Head and Neck Squamous Cell Carcinoma Cell Lines." Cellular Physiology and Biochemistry 36, no. 2 (2015): 784–98. http://dx.doi.org/10.1159/000430138.
Full textAbstract:
Background/Aims: Head and neck squamous cell carcinoma (HNSCC) ranks sixth worldwide for tumor-related mortality. A subpopulation of tumor cells, termed cancer stem cells (CSCs), has the ability to support cancer growth. Therefore, profiling CSC-enriched populations could be a reliable tool to study cancer biology. Methods: We performed phenotypic characterization of 7 HNSCC cell lines and evaluated the presence of CSCs. CSCs from Hep-2 cell line and HNSCC primary cultures were enriched through sphere formation and sphere-forming cells have been characterized both in vitro and in vivo. In addition, we investigated the expression levels of Nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed in several malignancies. Results: CSC markers were markedly expressed in Hep-2 cell line, which was found to be highly tumorigenic. CSC-enriched populations displayed increased expression of CSC markers and a strong capability to form tumors in vivo. We also found an overexpression of CSC markers in tumor formed by CSC-enriched populations. Interestingly, NNMT levels were significantly higher in CSC-enriched populations compared with parental cells. Conclusion: Our study provides an useful procedure for CSC identification and enrichment in HNSCC. Moreover, results obtained seem to suggest that CSCs may represent a promising target for an anticancer therapy.
39
Qiu, Zhenghua, Lingjing Tu, Xiongwei Hu, Zhipeng Zhou, Yongwei Lin, Lili Ye, and Chunhui Cui. "A Preliminary Study of miR-144 Inhibiting the Stemness of Colon Cancer Stem Cells by Targeting Krüppel-Like Factor 4." Journal of Biomedical Nanotechnology 16, no. 7 (July 1, 2020): 1102–9. http://dx.doi.org/10.1166/jbn.2020.2952.
Full textAbstract:
Colon cancer is a prevalent clinical malignant tumor of the digestive system. The current study aims to explore the miR-144 expression in colorectal cancer (CRC) cell lines and CRC stem cells (CSCs) and to explore its effect on the stemness of CSCs and the targeted regulation of Krüppel-like factor 4 (KLF4). Use qRT-PCR to detect the expression level of miR-144 in CRC cells SW480, HCT116, and H129 and the healthy colon cell NCM460. The CSCs that were used were cultured in HCT116 cells. Use western blot to explore the expressions of Nanog, SOX2, and OCT4 stemness marker protein. After it was transfected with miR-144 mimics or KLF4 plasmid, use MTT to explore the cell viability of CSCs, use flow cytometry to evaluate apoptosis, and use transwell assay to evaluate the ability of invasive of CSCs. The targeting effect of miR-144 on the KLF4 gene was verified using TargetScan prediction and the double-luciferase reporter gene test. Use qRT-PCR to evaluate the role of miR-144 mimics on KLF4 mRNA expression in CSCs. The qRT-PCR results exhibited that the miR-144 expression in CRC cells was higher than that in the healthy colon cell line. The expressions of OCT4, Nanog, and SOX2 stem cell markers were up-regulated in CSCs, and the expression of miR144 increased in CSCs. The cell viability, apoptosis, and invasion of CSCs increased after miR-144 was transfected. The TargetScan prediction and double-luciferase reporter gene assay confirmed that miR-144 was targeted by KLF4, and the expression of KLF4 mRNA in the miR-144 mimics group reduced. Moreover, the overexpression of KLF4 could partially reverse the role of miR-144 mimics on CSCs. In summary, miR-144 was highly expressed in CRC cell lines and CSCs, and the overexpression of miR-144 in CSCs significantly promoted the proliferation of CSCs, inhibited its apoptosis, and promoted its invasion ability. In addition, its preliminary mechanism, possibly through negative regulation KLF4, promotes the stemness of CSCs, and miR-144 is likely to be a potential target for eliminating CSC from CRC treatment.
40
Hubbard, Joleen M., and Axel Grothey. "Cancer Stem Cells and Cancer Stem Cell Inhibitors in Gastrointestinal Cancers." Oncology & Hematology Review (US) 12, no. 01 (2016): 41. http://dx.doi.org/10.17925/ohr.2016.12.01.41.
Full textAbstract:
Cancer stem cells (CSCs) are a subpopulation of phenotypically distinct cancer cells that may play an important role in tumor pathogenesis. The gastrointestinal (GI) system provides a good example for investigation of the role of CSCs in tumor proliferation; GI CSCs are suitable for study due to their abundance, proliferative potential, and consistent structural arrangement that is maintained under tightly controlled signaling pathways. GI stem cells have a long lifespan and this, combined with their rapid turnover, may predispose them to forming CSCs. Alternative possible sources of GI CSCs include differentiated intestinal cells, bone marrow, and cancer cells. Therapies that specifically target CSCs present an exciting opportunity to treat patients with cancer. Enhanced understanding of CSC markers, such as CD133, CD44, and epithelial cell adhesion molecule (EpCAM), may facilitate development of therapies that target them. Among the stemness pathways that have been targeted are Wnt/β-catenin, STAT, Notch, and Nanog.
41
Makki, Jaafar, Ohnmar Myint, Aye Aye Wynn, Ahmad Toha Samsudin, and John Daisy Vanitha. "Expression Distribution of Cancer Stem Cells, Epithelial to Mesenchymal Transition, and Telomerase Activity in Breast Cancer and Their Association with Clinicopathologic Characteristics." Clinical Medicine Insights: Pathology 8 (January 2015): CPath.S19615. http://dx.doi.org/10.4137/cpath.s19615.
Full textAbstract:
A total of 167 surgically resected primary invasive breast carcinomas and 63 metastatic lymph node lesions were analyzed for immunohistochemical (IHC) localization of the CD44+CD24_low breast cancer stem cell (CSC) markers, epithelial to mesenchymal transition (EMT) markers, and telomerase activity by double-staining IHC technique, in formalin-fixed, paraffin-embedded tissue, the results were validated by double-staining immunofluorescent and flow cytometry techniques. The results showed that CSCs with CD44+CD24_low phenotype were significantly increased in node-positive tumors, high-grade tumors, and ductal carcinoma in situ (DCIS). There was a high incidence of telomerase expression in metastatic lymph node lesion. There were considerably high number of tumor cells with EMT expression in metastatic lymph node lesion, and triple-negative tumor. The occurrence of EMT phenomena was usually accompanied by the co-existence of CSCs of CD44+CD24_low phenotype. There was no association between the existence of CSCs and detection of telomerase activity in tumor cells. Increased numbers of both CSCs of CD44+CD24_low phenotype and cells underwent EMT in DCIS lesion might be an initial step in the stromal invasion and propagation of breast cancer, and occurrence of EMT in the breast tumor associated with high prevalence of CSCs, promoting tumor invasiveness and metastasis.
42
Kushwaha, Prem Prakash, Shiv Verma, Shashank Kumar, and Sanjay Gupta. "Role of prostate cancer stem-like cells in the development of antiandrogen resistance." Cancer Drug Resistance 5, no. 2 (2022): 459–71. http://dx.doi.org/10.20517/cdr.2022.07.
Full textAbstract:
Androgen deprivation therapy (ADT) is the standard of care treatment for advance stage prostate cancer. Treatment with ADT develops resistance in multiple ways leading to the development of castration-resistant prostate cancer (CRPC). Present research establishes that prostate cancer stem-like cells (CSCs) play a central role in the development of treatment resistance followed by disease progression. Prostate CSCs are capable of self-renewal, differentiation, and regenerating tumor heterogeneity. The stemness properties in prostate CSCs arise due to various factors such as androgen receptor mutation and variants, epigenetic and genetic modifications leading to alteration in the tumor microenvironment, changes in ATP-binding cassette (ABC) transporters, and adaptations in molecular signaling pathways. ADT reprograms prostate tumor cellular machinery leading to the expression of various stem cell markers such as Aldehyde Dehydrogenase 1 Family Member A1 (ALDH1A1), Prominin 1 (PROM1/CD133), Indian blood group (CD44), SRY-Box Transcription Factor 2 (Sox2), POU Class 5 Homeobox 1(POU5F1/Oct4), Nanog and ABC transporters. These markers indicate enhanced self-renewal and stemness stimulating CRPC evolution, metastatic colonization, and resistance to antiandrogens. In this review, we discuss the role of ADT in prostate CSCs differentiation and acquisition of CRPC, their isolation, identification and characterization, as well as the factors and pathways contributing to CSCs expansion and therapeutic opportunities.
43
Lee-Theilen, Mieun, Delaine D. Fadini, Julia R. Hadhoud, Fleur van Dongen, Gabriela Kroll, Udo Rolle, and Henning C. Fiegel. "Hepatoblastoma Cancer Stem Cells Express PD-L1, Reveal Plasticity and Can Emerge upon Chemotherapy." Cancers 14, no. 23 (November 25, 2022): 5825. http://dx.doi.org/10.3390/cancers14235825.
Full textAbstract:
The biology of cancer stem cells (CSCs) of pediatric cancers, such as hepatoblastoma, is sparsely explored. This is mainly due to the very immature nature of these tumors, which complicates the distinction of CSCs from the other tumor cells. Previously, we identified a CSC population in hepatoblastoma cell lines expressing the CSC markers CD34 and CD90, cell surface Vimentin (csVimentin) and binding of OV-6. In this study, we detected the co-expression of the immune escape factor PD-L1 in the CSC population, whereas the other tumor cells remained negative. FACS data revealed that non-CSCs give rise to CSCs, reflecting plasticity of CSCs and non-CSCs in hepatoblastoma as seen in other tumors. When we treated cells with cisplatin and decitabine, a new CD34+/lowOV-6lowCD90+ population emerged that lacked csVimentin and PD-L1 expression. Expression analyses showed that this new CSC subset shared similar pluripotency and EMT features with the already-known CSCs. FACS results further revealed that this subset is also generated from non-CSCs. In conclusion, we showed that hepatoblastoma CSCs express PD-L1 and that the biology of hepatoblastoma CSCs is of a plastic nature. Chemotherapeutic treatment leads to another CSC subset, which is highly chemoresistant and could be responsible for a poor prognosis after postoperative chemotherapy.
44
Berber, Mohamed R., Hoda Elkhenany, Inas H. Hafez, Ahmed El-Badawy, Mohamed Essawy, and Nagwa El-Badri. "Efficient tailoring of platinum nanoparticles supported on multiwalled carbon nanotubes for cancer therapy." Nanomedicine 15, no. 8 (April 2020): 793–808. http://dx.doi.org/10.2217/nnm-2019-0445.
Full textAbstract:
Aim: Therapeutically targeting cancer stem cells (CSCs), which play a role in tumor initiation and relapse, remains challenging. Materials & methods: Novel-formulated platinum nanoparticles (Pt-NPs) supported on polybenzimidazole (PBI)-functionalized polymers and multiwalled carbon nanotubes (MWCNT) were prepared and their effect on CSCs was evaluated. Results: Pt-NPs showed homogenous distribution on the surface of MWCNT/PBI composites, with very narrow particle size. MWCNT/PBI/Pt-NPs resulted in a dramatic decrease in the proliferation rate of CSCs but not bone marrow mesenchymal stem cells (BM-MSCs). Quantitative gene expression analysis revealed that MWCNT/PBI/Pt had a significant inhibitory effect on the epithelial-mesenchymal transition and cell cycle markers of CSCs. Conclusion: MWCNT/PBI/Pt exhibited a specific cytotoxic effect on breast CSCs but not on adult stem cells.
45
Goto, Norihiro, Akihisa Fukuda, Yuichi Yamaga, Takaaki Yoshikawa, Takahisa Maruno, Hisatsugu Maekawa, Susumu Inamoto, et al. "Lineage tracing and targeting of IL17RB+tuft cell-like human colorectal cancer stem cells." Proceedings of the National Academy of Sciences 116, no. 26 (June 10, 2019): 12996–3005. http://dx.doi.org/10.1073/pnas.1900251116.
Full textAbstract:
Cancer stem cell (CSC)-specific markers may be potential therapeutic targets. We previously identified that Dclk1, a tuft cell marker, marks tumor stem cells (TSCs) in mouse intestinal adenomas. Based on the analysis of mouse Dclk1+tumor cells, we aimed to identify a CSC-specific cell surface marker in human colorectal cancers (hCRCs) and validate the therapeutic effect of targeting it. IL17RB was distinctively expressed by Dclk1+mouse intestinal tumor cells. UsingIl17rb-CreERT2-IRES-EGFPmice, we show that IL17RB marked intestinal TSCs in an IL13-dependent manner. Tuft cell-like cancer cells were detected in a subset of hCRCs. In these hCRCs, lineage-tracing experiments in CRISPR-Cas9–mediatedIL17RB-CreERT2knockin organoids and xenograft tumors revealed that IL17RB marks CSCs that expand independently of IL-13. We observed up-regulation ofPOU2F3, a master regulator of tuft cell differentiation, and autonomous tuft cell-like cancer cell differentiation in the hCRCs. Furthermore, long-term ablation of IL17RB-expressing CSCs strongly suppressed the tumor growth in vivo. These findings reveal insights into a CSC-specific marker IL17RB in a subset of hCRCs, and preclinically validate IL17RB+CSCs as a cancer therapeutic target.
46
Kong, Byung Ho, Ju Hyung Moon, Yong-Min Huh, Jin-Kyoung Shim, Ji-Hyun Lee, Eui-Hyun Kim, Jong Hee Chang, et al. "Prognostic Value of Glioma Cancer Stem Cell Isolation in Survival of Primary Glioblastoma Patients." Stem Cells International 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/838950.
Full textAbstract:
Cancer stem cells (CSCs) have been reported to be critical in the initiation, maintenance, and progression of cancers. The expression of stem cell markers, such as podoplanin (PDPN), CD133, and nestin, may have been correlated with malignant progression. However, the effects of CSCs and stem cell markers on clinical outcomes in cancer patients remain unclear. In this study, we assessed the prognostic roles of glioma CSCs (gCSCs) isolation and stem cell markers in patients with primary glioblastoma (pGBM). A cohort of 39 patients with pGBM was separated into two groups, those positive or negative for gCSCs, and the correlation between gCSC and patient survival was evaluated. We observed significantly different cumulative survival (P=0.045) when comparing patients positive for gCSCs patients and negative for gCSC. Among the patients positive for gCSCs, we observed no significant differences in survival between those whose gCSCs were each positive or negative for PDPN, CD133, or nestin. This study strongly supports the prognostic value of gCSCs isolation on the survival of patients with pGBM.
47
Peired, Anna Julie, Alessandro Sisti, and Paola Romagnani. "Renal Cancer Stem Cells: Characterization and Targeted Therapies." Stem Cells International 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/8342625.
Full textAbstract:
Renal cell carcinoma (RCC) is a major neoplasm with high incidence in western countries. Tumors are heterogeneous and are composed of differentiated cancer cells, stromal cells, and cancer stem cells (CSCs). CSCs possess two main properties: self-renewal and proliferation. Additionally, they can generate new tumors once transplanted into immunodeficient mice. Several approaches have been described to identify them, through the expression of cell markers, functional assays, or a combination of both. As CSCs are involved in the resistance mechanisms to radio- and chemotherapies, several new strategies have been proposed to directly target CSCs in RCC. One approach drives CSCs to differentiate into cancer cells sensitive to conventional treatments, while the other proposes to eradicate them selectively. A series of innovative therapies aiming at eliminating CSCs have been designed to treat other types of cancer and have not been experimented with on RCC yet, but they reveal themselves to be promising. In conclusion, CSCs are an important player in carcinogenesis and represent a valid target for therapy in RCC patients.
48
Minuk, Gerald Y., Wendy Bautista, and Julianne Klein. "Evidence of Hepatitis B Virus Infection in Cancer and Noncancer Stem Cells Associated with Human Hepatocellular Carcinoma." Canadian Journal of Infectious Diseases and Medical Microbiology 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/8931591.
Full textAbstract:
Both the hepatitis B virus (HBV) and cancer stem cells (CSCs) have been independently implicated in the pathogenesis of hepatocellular carcinoma (HCC). To date, there have been no reports describing HBV infection within CSCs. In this report we describe HBV core (HBcAg) and HBx protein expression within CSCs associated with human HCC. HBV markers were also identified in nonmalignant stem cells present in adjacent nontumor tissue. These findings provide new insights into the pathogenesis of HBV-induced HCC and are potentially relevant to the treatment of both HCC and chronic HBV.
49
Saito, Shigeo, Chia-Chen Ku, Kenly Wuputra, Jia-Bin Pan, Chang-Shen Lin, Ying-Chu Lin, Deng-Chyang Wu, and Kazunari K. Yokoyama. "Biomarkers of Cancer Stem Cells for Experimental Research and Clinical Application." Journal of Personalized Medicine 12, no. 5 (April 29, 2022): 715. http://dx.doi.org/10.3390/jpm12050715.
Full textAbstract:
The use of biomarkers in cancer diagnosis, therapy, and prognosis has been highly effective over several decades. Studies of biomarkers in cancer patients pre- and post-treatment and during cancer progression have helped identify cancer stem cells (CSCs) and their related microenvironments. These analyses are critical for the therapeutic application of drugs and the efficient targeting and prevention of cancer progression, as well as the investigation of the mechanism of the cancer development. Biomarkers that characterize CSCs have thus been identified and correlated to diagnosis, therapy, and prognosis. However, CSCs demonstrate elevated levels of plasticity, which alters their functional phenotype and appearance by interacting with their microenvironments, in response to chemotherapy and radiotherapeutics. In turn, these changes induce different metabolic adaptations of CSCs. This article provides a review of the most frequently used CSCs and stem cell markers.
50
Aramini, Beatrice, Valentina Masciale, Giulia Grisendi, Federica Bertolini, Michela Maur, Giorgia Guaitoli, Isca Chrystel, et al. "Dissecting Tumor Growth: The Role of Cancer Stem Cells in Drug Resistance and Recurrence." Cancers 14, no. 4 (February 15, 2022): 976. http://dx.doi.org/10.3390/cancers14040976.
Full textAbstract:
Emerging evidence suggests that a small subpopulation of cancer stem cells (CSCs) is responsible for initiation, progression, and metastasis cascade in tumors. CSCs share characteristics with normal stem cells, i.e., self-renewal and differentiation potential, suggesting that they can drive cancer progression. Consequently, targeting CSCs to prevent tumor growth or regrowth might offer a chance to lead the fight against cancer. CSCs create their niche, a specific area within tissue with a unique microenvironment that sustains their vital functions. Interactions between CSCs and their niches play a critical role in regulating CSCs’ self-renewal and tumorigenesis. Differences observed in the frequency of CSCs, due to the phenotypic plasticity of many cancer cells, remain a challenge in cancer therapeutics, since CSCs can modulate their transcriptional activities into a more stem-like state to protect themselves from destruction. This plasticity represents an essential step for future therapeutic approaches. Regarding self-renewal, CSCs are modulated by the same molecular pathways found in normal stem cells, such as Wnt/β-catenin signaling, Notch signaling, and Hedgehog signaling. Another key characteristic of CSCs is their resistance to standard chemotherapy and radiotherapy treatments, due to their capacity to rest in a quiescent state. This review will analyze the primary mechanisms involved in CSC tumorigenesis, with particular attention to the roles of CSCs in tumor progression in benign and malignant diseases; and will examine future perspectives on the identification of new markers to better control tumorigenesis, as well as dissecting the metastasis process.