Artykuły w czasopismach na temat „Cancer cells – Proliferation”
Kliknij ten link, aby zobaczyć inne rodzaje publikacji na ten temat: Cancer cells – Proliferation.
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Sprawdź 50 najlepszych artykułów w czasopismach naukowych na temat „Cancer cells – Proliferation”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Przeglądaj artykuły w czasopismach z różnych dziedzin i twórz odpowiednie bibliografie.
1
Kabraji, Sheheryar Kairas, Giorgio Gaglia, Danae Argyropoulou, Yang Dai, Shu Wang, Johann Bergholz, Shannon Coy i in. "Temporal and spatial topography of cell proliferation in cancer." Journal of Clinical Oncology 39, nr 15_suppl (20.05.2021): 3122. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.3122.
Pełny tekst źródłaStreszczenie:
3122 Background: Tumors are complex ecosystems where exogenous and endogenous cues are integrated to either stimulate or inhibit cancer cell proliferation. However, the nature of these complex cell cycle states, their spatial organization, response to perturbation, and implications for clinical outcomes, are poorly characterized in tumor tissues. Methods: We used multiplexed tissue imaging to develop a robust classifier of proliferation, the multivariate proliferation index (MPI), using 513 unique tumors across five cancer types. Next, we used dimensionality reduction analysis to assess how the patterns of cell cycle protein expression in tumors were altered in response to perturbation. Results: The MPI outperforms single markers, like Ki67, when classifying proliferative index across diverse tumor types and reveals the proliferative architecture of tumors in situ. We find that proliferative and non-proliferative cancer cells are organized across microscopic (cell-to-cell) and macroscopic (tissue-level) scales. Both domains are reshaped by therapy, and local clusters of proliferative and non-proliferative tumor cells preferentially neighbor distinct tumor-infiltrating immune cells. We further phenotyped non-proliferating cancer cells using markers of quiescent cancer cells, cancer stem cells, and dormant cancer cells. We found that these types of non-proliferating cancer cells can occupy distinct regions within the same primary tumor. In high-dimensional marker space, populations of proliferative cancer cells express canonical patterns of cell cycle protein markers, a property we refer to as “cell cycle coherence”. Untreated tumors exist in a continuum of coherence states, ranging from optimal coherence, akin to freely cycling cells in culture, to reduced coherence characterized by either cell cycle polarization or non-canonical marker expression. Coherence can be stereotypically altered by induction and abrogation of mitogen signaling in a HER2-driven model of breast cancer. Cell cycle coherence is modulated by neoadjuvant therapy in patients with localized breast cancer, and coherence is associated with disease-free survival after adjuvant therapy in patients with colorectal cancer, mesothelioma and glioblastoma. Conclusions: The MPI robustly defines proliferating and non-proliferating cells in tissues, with immediate implications for clinical practice and research. The coherence metrics capture the diversity of post-treatment cell cycle states directly in clinical samples, a fundamental step in advancing precision medicine. More broadly, replacing binary metrics with multivariate traits provides a quantitative framework to study temporal processes from fixed static images and to investigate the rich spatial biology of human cancers.
2
Cho, Min Soon, Justin Bottsford-Miller, Hernan G. Vasquez, Rebecca Stone, Behrouz Zand, Michael H. Kroll, Anil K. Sood i Vahid Afshar-Kharghan. "Platelets increase the proliferation of ovarian cancer cells". Blood 120, nr 24 (6.12.2012): 4869–72. http://dx.doi.org/10.1182/blood-2012-06-438598.
Pełny tekst źródłaStreszczenie:
Abstract Platelets promote metastasis and angiogenesis, but their effect on tumor cell growth is uncertain. Here we report a direct proliferative effect of platelets on cancer cells both in vitro and in vivo. Incubation of platelets with ovarian cancer cells from murine (ID8 and 2C6) or human (SKOV3 and OVCAR5) origin increased cell proliferation. The proliferative effect of platelets was not dependent on direct contact with cancer cells, and preincubation of platelets with blocking antibodies against platelet adhesion molecules did not alter their effect on cancer cells. The proliferative effect of platelets was reduced by fixing platelets with paraformaldehyde, preincubating platelets with a TGF-β1–blocking antibody, or reducing expression of TGF-βR1 receptor on cancer cells with siRNA. Infusing platelets into mice with orthotopic ovarian tumors significantly increased the proliferation indices in these tumors. Ovarian cancer patients with thrombocytosis had higher tumor proliferation indices compared with patients with normal platelet counts.
3
Cho, Minsoon, Justin Bottsford-Miller, Behrouz Zand, Hernan G. Vasquez, Rebecca L. Stone, Michael H. Kroll, Anil K. Sood i Vahid Afshar-Kharghan. "Platelets Promote Ovarian Cancer Growth: New Insights On Proliferation". Blood 120, nr 21 (16.11.2012): 96. http://dx.doi.org/10.1182/blood.v120.21.96.96.
Pełny tekst źródłaStreszczenie:
Abstract Abstract 96 Introduction. Platelets can promote metastasis by a multitude of effects. We have recently shown that reducing platelet counts decreased the size and number of tumor nodules in a murine model of orthotopic ovarian cancer. Here, we report a previously unrecognized pro-proliferative effects of platelets on ovarian cancer cells, using in vivo and in vitro assays. Methods and Results. The proliferation rate of human and murine ovarian cancer cells increased significantly after coincubation with platelets (Figure 1A). This effect was platelet-specific, as red blood cells did not alter the proliferation rate. Direct contact between platelets and cancer cells or intact platelets was not required for the proliferative response. Furthermore, platelets isolated from tumor-bearing mice were similar to platelets from control mice in their proliferative effect (Figure 1B). Blocking platelet adhesive surface proteins (GPIba, GPIIbb3, and P-selectin) did not diminish the proliferative effect of platelets (Figure 1C) and aspirin only partially inhibited it (Figure 1D). Fixation of platelets with paraformaldehye (2%) completely eliminated the effect of platelets on proliferation of cancer cells (Figure 1D). To determine mechanism, we examined the effect of blocking antibody to TGFb1 and identified a dose-dependent inhibition of the proliferative effect of platelets on ovarian cancer cells by the anti-TGF b1 antibody. To confirm results obtained with the TGF b1-blocking antibody, we reduced expression of TGFbR1 receptors on ovarian cancer cells with siRNA prior to their incubation with platelets (Figure 1E). Consistent with results observed following treatment with the TGFb1-blocking antibody, TGFbR1 siRNA reduced proliferation of ovarian cancer cells (Figure 1F). To study the effect of platelets in vivo, we injected syngeneic platelets into mice with orthotopic ovarian cancer on a weekly basis for four weeks, and measured the proliferation index in the resected tumors using Ki67 staining. We found that mice receiving platelet infusions had a significantly higher percentage of Ki67 positivity compared to control tumor-bearing mice (83.5% vs 66.3%, respectively; p<0.0005). To extend these findings to human disease, we next measured proliferation indices in 20 tumor specimens collected from patients with ovarian cancer. Ten of these patients had thrombocytosis (> 450,000/ml) and 10 had normal platelet counts with an average of 284,000/ml. Thrombocytosis was associated with a higher percentage of Ki67 positivity in tumors (68% vs, 57%, respectively; p=0.03). Summary and conclusion. In summary, platelets significantly increase the proliferation of ovarian cancer cells. These results provide a new understanding of mechanisms by which platelets contribute to tumor progression. Disclosures: Kroll: Aplagon: Membership on an entity's Board of Directors or advisory committees; Optimer: Consultancy; Leo: Honoraria, Travel Expenses, Travel Expenses Other.
4
Hubbard, Joleen M., i Axel Grothey. "Cancer Stem Cells and Cancer Stem Cell Inhibitors in Gastrointestinal Cancers". Oncology & Hematology Review (US) 12, nr 01 (2016): 41. http://dx.doi.org/10.17925/ohr.2016.12.01.41.
Pełny tekst źródłaStreszczenie:
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.
5
Harris, George, Raed Abu Ghazallah, David Nascene, Beverly Wuertz i Frank G. Ondrey. "PPAR Activation and Decreased Proliferation in Oral Carcinoma Cells With 4-HPR". Otolaryngology–Head and Neck Surgery 133, nr 5 (listopad 2005): 695–701. http://dx.doi.org/10.1016/j.otohns.2005.07.019.
Pełny tekst źródłaStreszczenie:
OBJECTIVE: To explore whether the mechanism of action of 4-hydroxyphenylretinamide (4-HPR, fenretidine), a synthetic retinoid, involves the functional activation of the nuclear hormone receptor class known as PPARs (peroxisome proliferator-activated receptors). Also, to examine whether anti-proliferative effects of this agent in head and neck cancer cells occur at biologically relevant concentrations. STUDY DESIGN/METHODS: CA 9–22, NA, and UM SCC 11B cells were treated with 4-HPR during their log phase growth and functional activation of PPAR γ was evaluated by plate luminometry. Cellular proliferation was analyzed by standard MTT cell proliferation assays and cell counting. Student's t tests were performed for all experiments. RESULTS: Significant dose-dependent increases in PPAR γ activation occurred in response to 4-HPR treatment. Proliferation was significantly inhibited by 4-HPR in a dose-dependent manner as judged by MTT and cell counting assays. These effects occurred at equimolar concentrations in both types of experiments within a range of clinically achievable doses (1–4 μM) of 4-HPR. CONCLUSIONS: 4-HPR can functionally activate PPAR γ at clinically achievable doses. Decreased cancer cell proliferation secondary to PPAR γ activation has been observed in other malignancies as well as upper aerodigestive cancer. PPAR γ activation by 4-HPR represents another potential anti-cancer mechanism of action for this drug. CLINICAL SIGNIFICANCE: PPAR γ activation represents a novel target for anti-cancer therapy for head and neck cancer and the current level of clinical toxicity of 4-HPR would be judged acceptable to utilize this agent alone or in combination chemotherapy.
6
Isazadeh, Alireza, Saba Hajazimian, Behrouz Shadman, Sahar Safaei, Ahmad Babazadeh Bedoustani, Reza Chavoshi, Dariush Shanehbandi, Mohammadreza Mashayekhi, Mohammadreza Nahaei i Behzad Baradaran. "Anti-Cancer Effects of Probiotic Lactobacillus acidophilus for Colorectal Cancer Cell Line Caco-2 through Apoptosis Induction". Pharmaceutical Sciences 27, nr 2 (2.10.2020): 262–67. http://dx.doi.org/10.34172/ps.2020.52.
Pełny tekst źródłaStreszczenie:
Background: Colorectal cancer is one of the most common cancers worldwide. Probiotics are useful and non-pathogenic microorganisms in the gastrointestinal tract, which can show anticancer activity through the induction of apoptosis. This study aimed to evaluate the antiproliferative effects of Lactobacillus acidophilus probiotic on the Caco-2 colorectal cancer cell line. Methods: The supernatant (secreted metabolites) and bacterial extract of L. acidophilus probiotics were prepared and used as an anti-proliferative agent on the colorectal cancer cell line, Caco-2 in vitro. The effects of supernatant and extract of L. acidophilus were evaluated on the viability and proliferation of cancer cells using MTT assay. Moreover, morphological alterations of cancer cells treated with supernatant and extract of L. acidophilus were evaluated by an inverted phase contrast microscope. The mRNA expression levels of apoptosis-related genes (SURVIVIN and SMAC) in treated cancer cells and untreated controls were evaluated using the Real-Time PCR method. Results: The results showed that the supernatant and extract of L. acidophilus inhibited the viability and proliferation of cancer cells in a dose and time-dependent manner. Moreover, various morphological alterations were observed in the treated cancer cells, which are indicators of apoptosis induction. The mRNA expression of SURVIVIN and SMAC genes were significantly up-regulated and downregulated in the treated cancer cells, respectively. Conclusion: The results of the present study suggested that the supernatant and extract of L.acidophilus could inhibit the viability and proliferation of colorectal cancer cell line, Caco-2through induction of apoptosis, increase the survival rate of colon cancer patients.
7
Chen, Qi, Victoria Rutten, Wei-Tzu Cheng, Mancy Tong, Jia Wei, Peter Stone, Lai-Ming Ching i Lawrence W. Chamley. "Phagocytosis of Extracellular Vesicles Extruded From the Placenta by Ovarian Cancer Cells Inhibits Growth of the Cancer Cells". International Journal of Gynecologic Cancer 28, nr 3 (marzec 2018): 545–52. http://dx.doi.org/10.1097/igc.0000000000001140.
Pełny tekst źródłaStreszczenie:
ObjectiveOvarian cancer is a common gynecological cancer, and parity is negatively associated with the incidence of this disease. This negative association is hypothesized to be due in part to shifting the balance of estrogen and progesterone toward more progesterone and reduced ovulation during pregnancy. However, studies suggested that parity is also associated with estrogen-independent gynecological cancers suggesting balance of hormones may not be the only protective factor. Extracellular vesicles (EVs) play an important role in cell-to-cell communication in physiological and pathological conditions. During pregnancy, large amounts of EVs are extruded from the placenta, and they seem to be involved in the remarkable adaptation of a woman's body to normal pregnancy. We hypothesized that EVs extruded from the placenta play a role in this protective effect.MethodsPlacental EVs were collected from first-trimester placentae, and cancer cell EVs were isolated from ovarian cancer cells. The EVs were exposed to ovarian cancer cells for 48 hours. The proliferation of cancer cells and the cell cycle were measured. In addition, phagocytosis of deported placental EVs by cancer cells was also measured.ResultsThe proliferation of cancer cells was significantly reduced by treatment with placental EVs (P = 0.001, analysis of variance), but not EVs from monocytes (P = 0.195), compared with untreated cancer cells. Furthermore, placental EVs also prevented the proliferation of cancer cells induced by cancer cell–derived EVs (P = 0.001). This inhibition of proliferation of ovarian cancer cells was partially due to phagocytosis of placental EVs by cancer cells. Phagocytosis of placental EVs delayed progression through the cell cycle. Calreticulin, a phagocytic “eat me” signal carried by placental EVs significantly inhibited ovarian cancer growth (P = 0.001).ConclusionsOur data demonstrated that EVs extruded from the placenta prevented ovarian cancer cell growth by a mechanism that involved delaying progression of the cell cycle after phagocytosis of the EVs.
8
Subramaniam, Kavita S., Seng Tian Tham, Zahurin Mohamed, Yin Ling Woo, Noor Azmi Mat Adenan i Ivy Chung. "Cancer-Associated Fibroblasts Promote Proliferation of Endometrial Cancer Cells". PLoS ONE 8, nr 7 (26.07.2013): e68923. http://dx.doi.org/10.1371/journal.pone.0068923.
Pełny tekst źródła
9
Paiboon, Nitchapon, Witchayaporn Kamprom, Sirikul Manochantr, Chairat Tantrawatpan, Duangrat Tantikanlayaporn, Sittiruk Roytrakul i Pakpoom Kheolamai. "Gestational Tissue-Derived Human Mesenchymal Stem Cells Use Distinct Combinations of Bioactive Molecules to Suppress the Proliferation of Human Hepatoblastoma and Colorectal Cancer Cells". Stem Cells International 2019 (4.07.2019): 1–15. http://dx.doi.org/10.1155/2019/9748795.
Pełny tekst źródłaStreszczenie:
Background. Cancer has been considered a serious global health problem and a leading cause of morbidity and mortality worldwide. Despite recent advances in cancer therapy, treatments of advance stage cancers are mostly ineffective resulting in poor survival of patients. Recent evidences suggest that multipotent human mesenchymal stem cells (hMSCs) play important roles in growth and metastasis of several cancers by enhancing their engraftment and inducing tumor neovascularization. However, the effect of hMSCs on cancer cells is still controversial because there are also evidences demonstrating that hMSCs inhibited growth and metastasis of some cancers. Methods. In this study, we investigated the effects of bioactive molecules released from bone marrow and gestational tissue-derived hMSCs on the proliferation of various human cancer cells, including C3A, HT29, A549, Saos-2, and U251. We also characterized the hMSC-derived factors that inhibit cancer cell proliferation by protein fractionation and mass spectrometry analysis. Results. We herein make a direct comparison and show that the effects of hMSCs on cancer cell proliferation and migration depend on both hMSC sources and cancer cell types and cancer-derived bioactive molecules did not affect the cancer suppressive capacity of hMSCs. Moreover, hMSCs use distinct combination of bioactive molecules to suppress the proliferation of human hepatoblastoma and colorectal cancer cells. Using protein fractionation and mass spectrometry analysis, we have identified several novel hMSC-derived factors that might be able to suppress cancer cell proliferation. Conclusion. We believe that the procedure developed in this study could be used to discover other therapeutically useful molecules released by various hMSC sources for a future in vivo study.
10
Futakuchi, Mitsuru, Kris Lami, Yuri Tachibana, Yukari Yamamoto, Masahiro Furukawa i Junya Fukuoka. "The Effects of TGF-β Signaling on Cancer Cells and Cancer Stem Cells in the Bone Microenvironment". International Journal of Molecular Sciences 20, nr 20 (15.10.2019): 5117. http://dx.doi.org/10.3390/ijms20205117.
Pełny tekst źródłaStreszczenie:
Background: Transforming growth factor-β (TGF-β) plays a key role in bone metastasis formation; we hypothesized the possible involvement of TGF-β in the induction of cancer stem cells (CSCs) in the bone microenvironment (micro-E), which may be responsible for chemo-resistance. Methods: Mouse mammary tumor cells were implanted under the dorsal skin flap over the calvaria and into a subcutaneous (subQ) lesions in female mice, generating tumors in the bone and subQ micro-Es. After implantation of the tumor cells, mice were treated with a TGF-β R1 kinase inhibitor (R1-Ki). Results: Treatment with R1-Ki decreased tumor volume and cell proliferation in the bone micro-E, but not in the subQ micro-E. R1-Ki treatment did not affect the induction of necrosis or apoptosis in either bone or subQ micro-E. The number of cells positive for the CSC markers, SOX2, and CD166 in the bone micro-E, were significantly higher than those in the subQ micro-E. R1-Ki treatment significantly decreased the number of CSC marker positive cells in the bone micro-E but not in the subQ micro-E. TGF-β activation of the MAPK/ERK and AKT pathways was the underlying mechanism of cell proliferation in the bone micro-E. BMP signaling did not play a role in cell proliferation in either micro-E. Conclusion: Our results indicated that the bone micro-E is a key niche for CSC generation, and TGF-β signaling has important roles in generating CSCs and tumor cell proliferation in the bone micro-E. Therefore, it is critically important to evaluate responses to chemotherapeutic agents on both cancer stem cells and proliferating tumor cells in different tumor microenvironments in vivo.
11
Tetsu, Osamu, i Frank McCormick. "Proliferation of cancer cells despite CDK2 inhibition". Cancer Cell 3, nr 3 (marzec 2003): 233–45. http://dx.doi.org/10.1016/s1535-6108(03)00053-9.
Pełny tekst źródła
12
Feng, Lei, Jie Li, Ling-Di Yan i Jian Tang. "RASSF1A Suppresses Proliferation of Cervical Cancer Cells". Asian Pacific Journal of Cancer Prevention 15, nr 14 (30.07.2014): 5917–20. http://dx.doi.org/10.7314/apjcp.2014.15.14.5917.
Pełny tekst źródła
13
Hevia, D., J. C. Mayo, I. Quiros i R. M. Sainz. "Beer constituents inhibit prostate cancer cells proliferation". European Journal of Cancer Supplements 6, nr 9 (lipiec 2008): 142. http://dx.doi.org/10.1016/s1359-6349(08)71719-1.
Pełny tekst źródła
14
Kloeters, Oliver, Helmut Friess, Nathalia Giese, Markus W. Buechler, Yalcin Cetin i Hasan Kulaksiz. "Uroguanylin inhibits proliferation of pancreatic cancer cells". Scandinavian Journal of Gastroenterology 43, nr 4 (styczeń 2008): 447–55. http://dx.doi.org/10.1080/00365520701746378.
Pełny tekst źródła
15
Volakaki, Aspasia-Athina, Daniel Lafkas, Eva Kassi, Andrew V. Schally, Athanasios G. Papavassiliou i Hippokratis Kiaris. "Essential role of p21/waf1 in the mediation of the anti-proliferative effects of GHRH antagonist JMR-132". Journal of Molecular Endocrinology 41, nr 5 (2.09.2008): 389–92. http://dx.doi.org/10.1677/jme-08-0106.
Pełny tekst źródłaStreszczenie:
GHRH, besides its neuroendocrine action in controlling the release of GH from the pituitary, stimulates the growth of various cancers in vivo and in vitro by direct mechanism(s). However, the molecular mechanism that mediates these proliferative effects of GHRH in extrapituitary tissues remains poorly characterized. In the present study, we investigated whether the tumor suppressor p21/waf1 is involved in the mediation of the proliferative effects of GHRH in A549 human lung cancer epithelial cells. Exposure of A549 cells to the GHRH antagonist JMR-132 caused a significant inhibition in the rate of cell proliferation. In A549 cells, GHRH suppressed while JMR-132 increased the levels of p21 expression in a dose-dependent manner. This suggests that GHRH could regulate p21 levels. We then evaluated whether p21 is required in A549 cells for the regulation of cell proliferation by GHRH. To this end, we knocked-down p21 expression in A549 cells by siRNA and assessed the effects of antagonist JMR-132 on cell proliferation. We found that the loss of p21 expression abolished the anti-proliferative effects of JMR-132. Suppression of p21 expression by siRNA in human HT29 colon cancer cells and non-transformed mouse osteoblasts KS483 also blocked the anti-proliferative effects of JMR-132 suggesting that the regulation of cell proliferation by GHRH is p21 dependent. These results shed light on the molecular mechanism of action of GHRH antagonists in tumor tissues and suggest that the antineoplastic activity of GHRH antagonists could be considered for the treatment of cancers expressing p21.
16
Kang, Sang, Sunmi Lee i Joanna Lee. "Cancer-Associated Function of 2-Cys Peroxiredoxin Subtypes as a Survival Gatekeeper". Antioxidants 7, nr 11 (11.11.2018): 161. http://dx.doi.org/10.3390/antiox7110161.
Pełny tekst źródłaStreszczenie:
Cancer cells are abnormal cells that do not comply with tissue homeostasis but undergo uncontrolled proliferation. Such abnormality is driven mostly by somatic mutations on oncogenes and tumor suppressors. Cancerous mutations show intra-tumoral heterogeneity across cancer types and eventually converge into the self-activation of proliferative signaling. While transient production of intracellular reactive oxygen species (ROS) is essential for cell signaling, its persistent production is cytotoxic. Thus, cancer cells require increased levels of intracellular ROS for continuous proliferation, but overexpress cellular peroxidase enzymes, such as 2-Cys peroxiredoxins, to maintain ROS homeostasis. However, suppression of 2-Cys peroxiredoxins has also been reported in some metastatic cancers. Hence, the cancer-associated functions of 2-Cys peroxiredoxins must be illuminated in the cellular context. In this review, we describe the distinctive signaling roles of 2-Cys peroxiredoxins beyond their intrinsic ROS-scavenging role in relation to cancer cell death and survival.
17
Häfliger, Pascal, i Roch-Philippe Charles. "The L-Type Amino Acid Transporter LAT1—An Emerging Target in Cancer". International Journal of Molecular Sciences 20, nr 10 (16.05.2019): 2428. http://dx.doi.org/10.3390/ijms20102428.
Pełny tekst źródłaStreszczenie:
Chronic proliferation is a major hallmark of tumor cells. Rapidly proliferating cancer cells are highly dependent on nutrients in order to duplicate their cell mass during each cell division. In particular, essential amino acids are indispensable for proliferating cancer cells. Their uptake across the cell membrane is tightly controlled by membrane transporters. Among those, the L-type amino acid transporter LAT1 (SLC7A5) has been repeatedly found overexpressed in a vast variety of cancers. In this review, we summarize the most recent advances in our understanding of the role of LAT1 in cancer and highlight preclinical studies and drug developments underlying the potential of LAT1 as therapeutic target.
18
Nishimura, R., i N. Arima. "Clinical significance of proliferative activity evaluated by MIB-1 in the treatment and postoperative follow-up of early breast cancer". Journal of Clinical Oncology 25, nr 18_suppl (20.06.2007): 21054. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.21054.
Pełny tekst źródłaStreszczenie:
21054 Background: To evaluate a clinical significance of proliferative activity in breast cancer, we studied relationships between proliferative activity and recurrence rate, the time of recurrence or adjuvant therapy. Methods: We analyzed 2448 patients with primary breast cancer between 1987 and 2004 in the Kumamoto City Hospital, and 437 cases out of the patients developed recurrence. Furthermore, the rate of recurrence before and after 1999 when postoperative adjuvant therapy (such as CEF or Taxanes) was started as standard treatment was investigated. Proliferative activity was judged by immunostaining for MIB-1. The fraction of proliferating cells was classified into 3 degrees (=19%, 20–49%, 50%=). Median observation period was 70 months. Results: 1) Distribution of patients by proliferation was as follows; =19%:1215 cases(50%), 20–49%: 870 cases(35%), or 50%=: 363 cases(15%). There was a significant relationship between proliferative activity and tumor size, nodal status, ER, PgR, p53 or HER2 status. 2) Multivariate analysis for disease-free survival revealed that a proliferative activity was one of significant factors in node-negative and positive cases. Recurrence rate was 11.6% in cases with low proliferation and 31.0% in high proliferation. The mean period from operation to recurrence in cases with low proliferation was 50.2 months, whereas 19.9 months in high proliferation (p<0.0001). Moreover, 74% of recurrent cases with high proliferation recurred within 2 years after operation, and there were few recurrences from the fifth year. 3) Patients with low proliferation frequently developed bone metastasis. In local recurrence, diffuse skin recurrence was often seen in cases with high proliferation. 4) The prognosis of patients in the later period (standard therapy group) was significantly better than that of patients in the earlier period, especially in high proliferation group. Conclusions: Proliferative activity might reflect aggressive behavior of breast cancer and predict the time of recurrence. The standard adjuvant therapy was effective in inhibiting early recurrence with high proliferation. It is important to take proliferative activity into consideration in the treatment and follow-up of breast cancer. No significant financial relationships to disclose.
19
Green, S. E., P. Chapman, J. Burn, A. D. Burt, M. Bennett, D. R. Appleton, J. S. Varma i J. C. Mathers. "Colonic epithelial cell proliferation in hereditary non-polyposis colorectal cancer". Gut 43, nr 1 (1.07.1998): 85–92. http://dx.doi.org/10.1136/gut.43.1.85.
Pełny tekst źródłaStreszczenie:
Background—Despite the recent discovery of four genes responsible for up to 90% of all cases of hereditary non-polyposis colorectal cancer (HNPCC), there will still be families in whom predictive testing is not possible. A phenotypic biomarker would therefore be useful. An upwards shift of the proliferative compartment in colonic crypts is reported to be one of the earliest changes in premalignant mucosa.Aims—To assess the role of crypt cell proliferation as a phenotypic biomarker in HNPCC.Patients—Thirty five patients at 50% risk of carrying the HNPCC gene (21 of whom subsequently underwent predictive testing and hence gene carrier status was known) and 18 controls.Methods—Crypt cell proliferation was measured at five sites in the colon using two different techniques. Labelling index was determined using the monoclonal antibody MIB1 and whole crypt mitotic index was measured using the microdissection and crypt squash technique. The distribution of proliferating cells within the crypts was also assessed.Results—There were no significant differences in the total labelling index or mean number of mitoses per crypt, nor in the distribution of proliferating cells within the crypt, between the study and control groups at any site. When the 21 patients in whom gene carrier status was known were analysed separately there were no significant differences in the measured indices of proliferation between the HNPCC gene carriers and non-gene carriers.Conclusion—Crypt cell proliferation is not a discriminative marker of gene carriage in HNPCC.
20
Yuk, Hyeong-Dong, Kyoung-Hwa Lee, Hye-Sun Lee, Seung-Hwan Jeong, Yongseok Kho, Chang-Wook Jeong, Hyeon-Hoe Kim, Ja-Hyeon Ku i Cheol Kwak. "PDLIM2 Suppression Inhibit Proliferation and Metastasis in Kidney Cancer". Cancers 13, nr 12 (15.06.2021): 2991. http://dx.doi.org/10.3390/cancers13122991.
Pełny tekst źródłaStreszczenie:
We evaluated the expression of PDLIM2 in human kidney cancer cell lines from primary or metastatic origins and found that PDLIM2 expression was highly elevated in metastatic kidney cancers. We evaluated the effect of PDLIM2 inhibition by RNA interference method. PDLIM2 knockdown showed the decreased proliferation and metastatic character in human metastatic kidney cancer cells. By repeated round of orthotopic injection of RenCa mouse kidney cancer cell line, we obtained metastatic prone mouse kidney cancer cell lines. PDLIM2 expression was highly expressed in these metastatic prone cells comparing parental cells. In addition, we evaluated the in vivo efficacy of PDLIM2 knockout on the tumor formation and metastasis of kidney cancer cells using a PDLIM2 knockout mice. The experimental metastasis model with tail vein injection and orthotopic metastasis model injected into kidney all showed reduced lung metastasis cancer formation in PDLIM2 knockout mice comparing control Balb/c mice. Overall, our findings indicate that PDLIM2 is required for cancer formation and metastasis in metastatic kidney cancer, indicating that PDLIM2 may be a new therapeutic target for metastatic kidney cancer.
21
Edwards, Iris J., i Joseph T. O'Flaherty. "Omega-3 Fatty Acids and PPARγin Cancer". PPAR Research 2008 (2008): 1–14. http://dx.doi.org/10.1155/2008/358052.
Pełny tekst źródłaStreszczenie:
Omega-3 (or n-3) polyunsaturated fatty acids (PUFAs) and their metabolites are natural ligands for peroxisome proliferator receptor activator (PPAR)γand, due to the effects of PPARγon cell proliferation, survival, and differentiation, are potential anticancer agents. Dietary intake of omega-3 PUFAs has been associated with a reduced risk of certain cancers in human populations and in animal models. In vitro studies have shown that omega-3 PUFAs inhibit cell proliferation and induce apoptosis in cancer cells through various pathways but one of which involves PPARγactivation. The differential activation of PPARγand PPARγ-regulated genes by specific dietary fatty acids may be central to their distinct roles in cancer. This review summarizes studies relating PUFAs to PPARγand cancer and offers a new paradigm relating an n-3 PUFA through PPARγto the expression of the cell surface proteoglycan, syndecan-1, and to the death of cancer cells.
22
Preciado, Julian Adolfo, Eduardo Reátegui, Samira M. Azarin, Emil Lou i Alptekin Aksan. "Immobilization platform to induce quiescence in dormancy-capable cancer cells". TECHNOLOGY 05, nr 03 (wrzesień 2017): 129–38. http://dx.doi.org/10.1142/s2339547817500078.
Pełny tekst źródłaStreszczenie:
Cancer dormancy emerges when tumor cells cease to proliferate but remain alive in a quiescent state. Recent evidence suggests that cancer cells can stay dormant in a patient’s body for years before returning to a proliferative state, leading to cancer relapse. The lack of a system to efficiently identify and study dormant cancer cells is currently limiting further diagnostic and treatment developments to prevent cancer relapse. Herein, we present a novel encapsulation platform to identify and study dormancy-capable cancer cells in a quiescent state by inhibiting proliferation through physical confinement. The platform involves the encapsulation of cells within a stiff silica-PEG hydrogel produced by a sol–gel technique. Cells are immobilized in a nondegradable microenvironment where proliferation and movement are inhibited due to physical confinement of the gel. The platform was tested using non-cancerous cell lines HFF, HUVEC, Jurkat, MEF, and MCF-10A, and cancer cell lines LnCAP, MCF-7, MCF10DCIS.com , MDA-MB-468, and OVCAR-5. Viability and metabolic activity measurements showed that MCF-7, LnCAP, and MCF10DCIS.COM cells remained metabolically active for up to 3 weeks while non-cancerous lines and the rest of the cancer cell lines did not survive after a few days. Ki-67 immunofluorescent staining confirmed that surviving MCF-7 cells underwent cell cycle arrest as early as 48 hours after encapsulation. Furthermore, following extraction and recovery, these cells resumed proliferation, indicating that the induced cell cycle arrest was reversible. These results conclude that physically inhibiting proliferation via the silica-PEG hydrogel system can be used to identify cells that can enter a quiescent state, setting the groundwork for this platform to be explored as a cancer cell dormancy model.
23
Nair, Sangeeta, HoVan Nguyen, Salama Salama i Ayman Al-Hendy. "Obesity and the Endometrium: Adipocyte-Secreted Proinflammatory TNFαCytokine Enhances the Proliferation of Human Endometrial Glandular Cells". Obstetrics and Gynecology International 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/368543.
Pełny tekst źródłaStreszczenie:
Obesity, a state of chronic inflammation, is associated with poor fertility and low implantation rates and is a well-documented risk factor for endometrial cancer. Adipokines, such as tumor necrosis factor alpha, play an important role in initiation of endometrial cancer. The aim of this study is to evaluatein vitroeffects of human adipocyte cells (SW872) on growth of endometrial glandular epithelial cells (EGE).Methods.We measured cell proliferation and expression of cell-growth proteins—proliferating cell nuclear antigen, cyclin D1, cyclin-dependent kinase-1, and apoptotic markers (BCL-2 and BAK) in human EGE cells cocultured with SW872 cells. EGE cells were also evaluated in SW872-conditioned media neutralized with anti-TNFαantibody.Results.A significant increase in EGE cell proliferation was observed in both SW872-conditioned media and in coculture (P<0.05). We observed an upregulation of proliferation markers PCNA, cyclin D1, CDK-1, and BCL-2 and decrease in BAK (P<0.05). Neutralization of SW872-conditioned media using anti-TNFαantibodies reversed EGE cell proliferation as indicated by BCL-2 expression.Conclusions.Adipocytes have potent proliferative paracrine effect on EGE cells which may be, in part, mediated via TNFα. Further understanding of the role of obesity in endometrial carcinogenesis should lead to better preventative and therapeutic strategies.
24
Kim, Ki-Yon, Kyung-Chul Choi, Nelly Auersperg i Peter C. K. Leung. "Mechanism of gonadotropin-releasing hormone (GnRH)-I and -II-induced cell growth inhibition in ovarian cancer cells: role of the GnRH-I receptor and protein kinase C pathway". Endocrine-Related Cancer 13, nr 1 (marzec 2006): 211–20. http://dx.doi.org/10.1677/erc.1.01033.
Pełny tekst źródłaStreszczenie:
In our previous studies, we demonstrated that ERK1/2 (extracellular signal-regulated protein kinase) and p38 MAPK (mitogen-activated protein kinase) are required for gonadotropin-releasing hormone (GnRH)-II-induced anti-proliferation of ovarian cancer cells. In the present study, we examined the role of the GnRH-I receptor, as well as the activation of protein kinase C (PKC), in the anti-proliferative effect induced by GnRH-I or II in ovarian cancer cells. Our results demonstrated that Antide, a GnRH-I antagonist, reversed the activation of ERK1/2 induced by GnRH-I or II and abolished the anti-proliferative effect of GnRH-I and II in ovarian cancer cells. Transfection of short-interfering RNA to abrogate the gene expression of the GnRH-I receptor reversed GnRH-I and II-induced anti-proliferation. These results indicate that GnRH-I or II induce anti-proliferation through the GnRH-I receptor in ovarian cancer cells. In addition, the activation of ERK1/2 by GnRH-I or II was mimicked by phorbol-12-myristate 13-acetate, a PKC activator. Pretreatment with GF109203X, an inhibitor of PKC, blocked GnRH-induced ERK1/2 activation and anti-proliferation. These results suggest that the activation of PKC is responsible for GnRH-induced ERK1/2 activation and anti-proliferation in ovarian cancer cells. Taken together, these results indicate that binding of GnRH-I and II to the GnRH-I receptor activates ERK1/2 through a PKC-dependent pathway and is essential for GnRH-induced anti-proliferation of ovarian cancer cells.
25
Pan, Bin, Yunlin Ye, Haiping Liu, Jianli Zhen, Hongmei Zhou, Yutong Li, Lijun Qu, Youke Wu, Chuanrong Zeng i Weifeng Zhong. "URG11 Regulates Prostate Cancer Cell Proliferation, Migration, and Invasion". BioMed Research International 2018 (31.05.2018): 1–10. http://dx.doi.org/10.1155/2018/4060728.
Pełny tekst źródłaStreszczenie:
Upregulated gene 11 (URG11), a new gene upregulated by hepatitis B virus X protein, is involved in the development and progression of several tumors, including liver, stomach, lung, and colon cancers. However, the role of URG11 in prostate cancer remains yet to be elucidated. By determined expression in human prostate cancer tissues, URG11 was found significantly upregulated and positively correlated with the severity of prostate cancer, compared with that in benign prostatic hyperplasia tissues. Further, the mRNA and protein levels of URG11 were significantly upregulated in human prostate cancer cell lines (DU145, PC3, and LNCaP), compared with human prostate epithelial cell line (RWPE-1). Moreover, by the application of siRNA against URG11, the proliferation, migration, and invasion of prostate cancer cells were markedly inhibited. Genetic knockdown of URG11 also induced cell cycle arrest at G1/S phase, induced apoptosis, and decreased the expression level of β-catenin in prostate cancer cells. Overexpression of URG11 promoted the expression of β-catenin, the growth, the migration, and invasion ability of prostate cancer cells. Taken together, this study reveals that URG11 is critical for the proliferation, migration, and invasion in prostate cancer cells, providing the evidence of URG11 to be a novel potential therapeutic target of prostate cancer.
26
Franzè, Eleonora, Carmine Stolfi, Edoardo Troncone, Patrizio Scarozza i Giovanni Monteleone. "Role of Interleukin-34 in Cancer". Cancers 12, nr 1 (20.01.2020): 252. http://dx.doi.org/10.3390/cancers12010252.
Pełny tekst źródłaStreszczenie:
Cross-talk between cancer cells and the immune cells occurring in the tumor microenvironment is crucial in promoting signals that foster tumor growth and metastasis. Both cancer cells and immune cells secrete various interleukins (IL), which, either directly or indirectly, stimulate cancer-cell proliferation, survival, and diffusion, as well as contribute to sculpt the immune microenvironment, thereby amplifying tumorigenic stimuli. IL-34, a cytokine produced by a wide range of cells, has been initially involved in the control of differentiation, proliferation, and survival of myeloid cells. More recent studies documented the overexpression of IL-34 in several cancers, such as hepatocarcinoma, osteosarcoma, multiple myeloma, colon cancer, and lung cancer, and showed that tumor cells can produce and functionally respond to this cytokine. In this review, we summarize the multiple roles of IL-34 in various cancers, with the aim to better understand the relationship between the expression of this cytokine and cancer behavior and to provide new insights for exploring a new potential therapeutic target.
27
Lee, Jinseon, So-Jung Choi, Jhingook Kim i Sung-Hyun Kim. "Effect of cancer-associated fibroblasts on cell proliferation and resistance to EGFR-TKI in direct coculture with lung cancer cell lines." Journal of Clinical Oncology 30, nr 15_suppl (20.05.2012): e18083-e18083. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e18083.
Pełny tekst źródłaStreszczenie:
e18083 Background: Identical lung cancer cells may get diversified depending on tumor microenvironments. We hypothesized that diversity of cancer associated fibroblasts renders identical lung cancer cells various tumor characteristics such as drug responsiveness and proliferation rate. To test this hypothesis, we isolated cancer associated fibroblasts from 20 different lung cancers, and compared their effects on the proliferation and drug responsiveness of lung cell lines. Methods: Cancer associated fibroblasts were isolated from 20 solid tumors of NSCLCs, and treated with Mitomycin to control the overgrowth during cocultures. H358 and A549 cells were mixed with cancer associated fibroblasts in 1:1 ratio and co-cultured for 4-7 days. Cell number was scored by time-lapse photography, and cell morphology was observed under fluorescent microscope. Expression of cell type markers were examined. Responsiveness to Erlotinib was examined in coculture condistions. Results: Cancer associated fibroblasts stimulated cancer cell proliferation ranging from almost no effects to approximately 3 folds. Coculture in transwell with no direct contacts with cancer cells showed minimal stimulatory effects. Direct contacts induced dramatic changes in cancer cell morphology from cohesive epithelial colonies to dispersed fibroblastic single cells. EMT markers such as down-regulation of Cytokeratins and up-regulation of Vimentin were detected in GFP positive cells. A549 cells that were sensitive to 15 uM Erlotinib (IC50=7.5uM) became resistant when co-cultured with cancer associated fibroblasts. Conclusions: In this study, cancer associated fibroblasts isolated from different lung cancers induced significant changes in tumor cell characteristics such as proliferation, EMT, and drug responsiveness.
28
Li, Jing, Weixing Qu, Yazhou Jiang, Yi Sun, Yongyi Cheng, Tiejun Zou i Shuangkuan Du. "miR-489 Suppresses Proliferation and Invasion of Human Bladder Cancer Cells". Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 24, nr 6 (27.10.2016): 391–98. http://dx.doi.org/10.3727/096504016x14666990347518.
Pełny tekst źródłaStreszczenie:
MicroRNAs (miRNAs) have been shown to be involved in bladder cancer progression. miR-489 (also known as miR-489-3p) was recently reported to be a tumor suppressor in several cancers. However, its exact role and mechanism in the progression of bladder cancer are largely unknown. In this study, we explore the role of miR-489 in the proliferation and invasion of human bladder cancer cells. The miR-489 expression levels were detected in bladder cancer and normal adjacent tissues, as well as in human normal bladder epithelial cells and bladder cancer cell lines. The results showed that miR-489 was sharply reduced in bladder cancer tissues and cell lines. Then the miR-489 mimic or oligo anta-miR-489 was transfected into T24 and UMUC3 bladder cancer cell lines. The results showed that the miR-489 mimic greatly increased the miR-489 level and significantly decreased the proliferation and invasion of T24 and UMUC3 cells. In contrast, the anta-miR-489 had a completely opposite effect on miR-489 expression, cell proliferation, and cell invasion. Moreover, bioinformatics and luciferase reporter gene assays confirmed that miR-489 targeted the mRNA 3′-untranslated region (3′-UTR) region of Jagged1 (JAG1), a Notch ligand. In conclusion, miR-489 suppressed proliferation and invasion of human bladder cancer cells.
29
Hasan, Mahmud, Erin Browne, Laura Guarinoni, Travis Darveau, Katherine Hilton i Paula A. Witt-Enderby. "Novel Melatonin, Estrogen, and Progesterone Hormone Therapy Demonstrates Anti-Cancer Actions in MCF-7 and MDA-MB-231 Breast Cancer Cells". Breast Cancer: Basic and Clinical Research 14 (styczeń 2020): 117822342092463. http://dx.doi.org/10.1177/1178223420924634.
Pełny tekst źródłaStreszczenie:
A novel melatonin, estrogen, and progesterone hormone therapy was developed as a safe bio-identical alternative hormone therapy for menopausal women based on the Women’s Health Initiative findings that PremPro™ increased breast cancer risk and mortality of all types of breast cancer in postmenopausal women. For HER2 breast cancer, melatonin, estrogen, and progesterone delayed tumor onset and reduced tumor incidence in neu female mice. For other breast cancers, its actions are unknown. In this study, melatonin, estrogen, and progesterone hormone therapy were assessed in human ER+ (MCF-7) and triple negative breast cancer (MDA-MB-231) cells, and found to decrease proliferation and migration of both breast cancer lines. Inhibition of MEK1/2 and 5 using PD98059 and BIX02189, respectively, inhibited proliferation and migration in MDA-MB-231 cells and proliferation in MCF-7 cells; however, when combined with melatonin, estrogen, and progesterone, BIX02189 blocked melatonin, estrogen, and progesterone–mediated inhibition of migration in MCF-7 cells and induced Elf-5. For MDA-MB-231 cells, BIX02189 combined with melatonin, estrogen, and progesterone inhibited proliferation and increased pERK1/2 and β1-INTEGRIN; levels of pERK5 remained low/nearly absent in both breast cancer lines. These findings demonstrate novel anti-cancer actions of melatonin, estrogen, and progesterone in ER+ and triple negative breast cancer cells through intricate MEK1/2- and MEK5-associated signaling cascades that favor anti-proliferation and anti-migration.
30
Sazonov, S., A. Brilliant i Y. Brilliant. "Proliferation of cancer stem cells in triple negative breast cancer". Breast 32 (marzec 2017): S29—S30. http://dx.doi.org/10.1016/s0960-9776(17)30123-6.
Pełny tekst źródła
31
Stohnii, Y. M., M. V. Ryzhykova, A. V. Rebriev, M. D. Kuchma, R. Y. Marunych, V. O. Chernyshenko, V. A. Shablii i in. "Aggregation of platelets, proliferation of endothelial cells and motility of cancer cells are mediated by the B?1(15)-42 residue of fibrin(ogen)". Ukrainian Biochemical Journal 92, nr 2 (17.04.2020): 72–84. http://dx.doi.org/10.15407/ubj92.02.072.
Pełny tekst źródła
32
A, Mostafa. "Charactor of JNK and P53 in Taxol-Induced Apoptotic Signaling in SKOV3 Human Ovarian Cancer Cell Proliferation". Cancer Research and Cellular Therapeutics 1, nr 3 (8.09.2017): 01–07. http://dx.doi.org/10.31579/2640-1053/017.
Pełny tekst źródłaStreszczenie:
C-Jun N-terminal kinase (JNK) represents a group of mitogen-activated protein kinases (MAPKs) involved in many cellular responses including apoptosis. We have previously reported that taxol, a microtubule-interfering therapeutic agent widely used against various cancers, induces caspase-independent but apoptotic inducing factor (AIF)-dependent apoptosis in human ovarian cancer cell line SKOV3 cells. In the present study, we add to this report a detailed analysis of the taxol-induced apoptotic mechanisms in SKOV3 cells, particularly focusing on JNK and p53. In line with the previous report, we found that taxol induced caspase-independent apoptosis with concurrent activation of JNK, phosphorylation of Bcl-2, Bax translocation to the mitochondria, and AIF release from the mitochondria. Restoration of p53 functionality into SKOV3 cells, which are p53-null cells, by transfection of wild-type p53, however, induced caspase-dependent apoptosis in response to taxol treatment as evidenced by increasing PARP cleavage and the emergence of processed, active caspase-3 and -7. More to the point, treatment with a JNK inhibitor SP600125 blocked taxol-induced apoptotic cell death in both parental SKOV3 cells (p53-deficient) and p53-transfectant cells. Collectively, the aforementioned findings lend support to the view that taxol-induced apoptotic cell death in SKOV3 cells is executed by different mechanisms depending on the presence of p53 but commonly mediated by ASK1-JNK and/or -p38 axes.
33
Bahari, N. N., S. Y. N. Jamaludin, A. H. Jahidin, M. N. Zahary i A. B. Mohd Hilmi. "Assessment of TRPV4 Channel and Its Role in Colorectal Cancer Cells". Biomedical and Pharmacology Journal 12, nr 2 (18.06.2019): 629–38. http://dx.doi.org/10.13005/bpj/1683.
Pełny tekst źródłaStreszczenie:
The transient receptor potential vanilloid member 4 (TRPV4) is a non-selective calcium (Ca2+)-permeable channel which is widely expressed in different types of tissues including the lungs, liver, kidneys and salivary gland. TRPV4 has been shown to serve as a cellular sensor where it is involved in processes such as osmoregulation, cell volume regulation and thermoregulation. Emerging evidence suggests that TRPV4 also plays important roles in several aspects of cancer progression. Despite the reported roles of TRPV4 in several forms of cancers, the role of TRPV4 in human colorectal cancer remains largely unexplored. In the present study, we sought to establish the potential role of TRPV4 in colorectal cancer by assessing TRPV4 expression levels and investigating whether TRPV4 pharmacological modulation may alter cell proliferation, cell cycle and cell death in colorectal cancer cells. Quantitative real-time PCR analysis revealed that TRPV4 mRNA levels were significantly lower in HT-29 cells than normal colon CCD-18Co cells. However, TRPV4 mRNA was absent in HCT-116 cells. Pharmacological activation of TRPV4 with GSK1016790A significantly enhanced the proliferation of HT-29 cells while TRPV4 inhibition using RN 1734 decreased their proliferation. Increased proliferation in GSK1016790A-treated HT-29 cells was attenuated by co-treatment with RN 1734. Pharmacological modulation of TRPV4 had no effect on the cell cycle progression but promoted cell death in HT-29 cells. Taken together, these findings suggest differential TRPV4 expression levels in human colorectal cancer cells and that pharmacological modulation of TRPV4 produces distinct effects on the proliferation and induces cell death in HT-29 cells.
34
Jensen, Kirk, Athanasios Bikas, Aneeta Patel, Yevgeniya Kushchayeva, John Costello, Dennis McDaniel, Kenneth Burman i Vasyl Vasko. "Nelfinavir inhibits proliferation and induces DNA damage in thyroid cancer cells". Endocrine-Related Cancer 24, nr 3 (marzec 2017): 147–56. http://dx.doi.org/10.1530/erc-16-0568.
Pełny tekst źródłaStreszczenie:
The HIV protease inhibitor Nelfinavir (NFV) inhibits PI3K/AKT and MAPK/ERK signaling pathways, emerging targets in thyroid cancers. We examined the effects of NFV on cancer cells that derived from follicular (FTC), papillary (PTC) and anaplastic (ATC) thyroid cancers. NFV (1–20 µM) was tested in FTC133, BCPAP and SW1736 cell lines. The effects of NFV on cell proliferation were determined in vitro using real-time microscopy and by flow cytometry. DNA damage, apoptotic cell death and expression of molecular markers of epithelial–mesenchymal transition (EMT) were determined by Western blot and real-time PCR. Real-time imaging demonstrated that NFV (10 µM) increased the time required for the cell passage through the phases of cell cycle and induced DNA fragmentation. Growth inhibitory effects of NFV were associated with the accumulation of cells in G0/G1 phase, downregulation of cyclin D1 and cyclin-dependent kinase 4 (CDK4). NFV also induced the expression of γH2AX and p53BP1 indicating DNA damage. Treatment with NFV (20 µM) resulted in caspase-3 cleavage in all examined cells. NFV (20 µM) decreased the levels of total and p-AKT in PTEN-deficient FTC133 cells. NFV had no significant effects on total ERK and p-ERK in BRAF-positive BCPAP and SW1736 cells. NFV had no effects on the expression of EMT markers (Twist, Vimentin, E- and N-Cadherin), but inhibited the migration and decreased the abilities of thyroid cancer cells to survive in non-adherent conditions. We conclude that NFV inhibits proliferation and induces DNA damage in thyroid cancer cell lines. Our in vitro data suggest that NFV has a potential to become a new thyroid cancer therapeutic agent.
35
Lorenzo-Anota, Helen Yarimet, Diana G. Zarate-Triviño, Jorge Alberto Uribe-Echeverría, Andrea Ávila-Ávila, José Raúl Rangel-López, Ana Carolina Martínez-Torres i Cristina Rodríguez-Padilla. "Chitosan-Coated Gold Nanoparticles Induce Low Cytotoxicity and Low ROS Production in Primary Leucocytes, Independent of Their Proliferative Status". Pharmaceutics 13, nr 7 (24.06.2021): 942. http://dx.doi.org/10.3390/pharmaceutics13070942.
Pełny tekst źródłaStreszczenie:
(1) Background: Chitosan-coated gold nanoparticles (CH-AuNPs) have important theranostic applications in biomedical sciences, including cancer research. However, although cell cytotoxicity has been studied in cancerous cells, little is known about their effect in proliferating primary leukocytes. Here, we assessed the effect of CH-AuNPs and the implication of ROS on non-cancerous endothelial and fibroblast cell lines and in proliferative lymphoid cells. (2) Methods: The Turkevich method was used to synthetize gold nanoparticles. We tested cell viability, cell death, ROS production, and cell cycle in primary lymphoid cells, compared with non-cancer and cancer cell lines. Concanavalin A (ConA) or lipopolysaccharide (LPS) were used to induce proliferation on lymphoid cells. (3) Results: CH-AuNPs presented high cytotoxicity and ROS production against cancer cells compared to non-cancer cells; they also induced a different pattern of ROS production in peripheral blood mononuclear cells (PBMCs). No significant cell-death difference was found in PBMCs, splenic mononuclear cells, and bone marrow cells (BMC) with or without a proliferative stimuli. (4) Conclusions: Taken together, our results highlight the selectivity of CH-AuNPs to cancer cells, discarding a consistent cytotoxicity upon proliferative cells including endothelial, fibroblast, and lymphoid cells, and suggest their application in cancer treatment without affecting immune cells.
36
Lv, Yuanjing, Jinle Lu, Xin Liu, Susheng Miao, Xionghui Mao, Baojun Li, Rong Pei i Cheng Xiang. "Histone deacetylase 1 regulates the malignancy of oral cancer cells via miR-154-5p/PCNA axis". Biological Chemistry 401, nr 11 (25.10.2020): 1273–81. http://dx.doi.org/10.1515/hsz-2020-0189.
Pełny tekst źródłaStreszczenie:
AbstractHistone deacetylases (HDACs) can regulate the progression of various cancers, while their roles in oral cancer cells are not well known. Our present study found that the HDAC1 was over expressed in oral squamous cell carcinoma (OSCC) cells and tissues. Targeted inhibition of HDAC1 via its specific inhibitor PCI24781 or siRNA can inhibit the proliferation of OSCC cells and increase their sensitivity to the chemo-sensitivity such as doxorubicin treatment. HDAC1 can regulate the expression of proliferating cell nuclear antigen (PCNA) via decreasing its mRNA stability. While over expression of PCNA can attenuate HDAC1 inhibition induced suppression of cell proliferation. We checked the expression of various miRNAs which can target the 3′UTR of PCNA. Results showed that HDAC1 can negative regulate the expression of miR-154-5p, inhibitor of miR-154-5p can attenuate PCI24781 treatment decreased PCNA expression and cell proliferation. Collectively, our present study suggested that HDAC1 can promote the growth and progression of OSCC via regulation of miR-154-5p/PCNA signals.
37
Xu, Zengtao, Xiuping Chen, Shu Fu, Jiaolin Bao, Yuanye Dang, Mingqing Huang, Lidian Chen i Yitao Wang. "Dehydrocorydaline Inhibits Breast Cancer Cells Proliferation by Inducing Apoptosis in MCF-7 Cells". American Journal of Chinese Medicine 40, nr 01 (styczeń 2012): 177–85. http://dx.doi.org/10.1142/s0192415x12500140.
Pełny tekst źródłaStreszczenie:
Dehydrocorydaline is an alkaloid isolated from traditional Chinese herb Corydalis yanhusuo W.T. Wang. We discovered that it possessed anti-tumor potential during screening of anti-tumor natural products from Chinese medicine. In this study, its anti-tumor potential was investigated with breast cancer line cells MCF-7 in vitro. The anti-proliferative effect of dehydrocorydaline was determined by MTT assay and the mitochondrial membrane potential (Δ Ψ m) was monitored by JC-1 staining. DNA fragments were visualized by Hoechst 33342 staining and DNA ladder assay. Apoptotic related protein expressions were measured by Western blotting. Dehydrocorydaline significantly inhibited MCF-7 cell proliferation in a dose- dependent manner, which could be reversed by a caspase-8 inhibitor, Z-IETD-FMK. Dehydrocorydaline increased DNA fragments without affecting ΔΨm. Western blotting assay showed that dehydrocorydaline dose-dependently increased Bax protein expression and decreased Bcl-2 protein expression. Furthermore, dehydrocorydaline induced activation of caspase-7,-8 and the cleavage of PARP without affecting caspase-9. These results showed that dehydrocorydaline inhibits MCF-7 cell proliferation by inducing apoptosis mediated by regulating Bax/Bcl-2, activating caspases as well as cleaving PARP.
38
Czeczuga-Semeniuk, Ewa, Tomasz Anchim, Janusz Dziecioł, Milena Dabrowska i Sławomir Wołczyński. "Can transforming growth factor-beta1 and retinoids modify the activity of estradiol and antiestrogens in MCF-7 breast cancer cells?." Acta Biochimica Polonica 51, nr 3 (30.09.2004): 733–45. http://dx.doi.org/10.18388/abp.2004_3558.
Pełny tekst źródłaStreszczenie:
Retinoic acid and transforming growth factor-beta (TGF-beta) affect differentiation, proliferation and carcinogenesis of epithelial cells. The effect of both compounds on the proliferation of cells of the hormone sensitive human breast cancer cell line (ER+) MCF-7 was assessed in the presence of estradiol and tamoxifen. The assay was based on [3H]thymidine incorporation and the proliferative activity of PCNA- and Ki 67-positive cells. The apoptotic index and expression of the Bcl-2 and p53 antigens in MCF-7 cells were also determined. Exogenous TGF-beta1 added to the cell culture showed antiproliferative activity within the concentration range of 0.003-30 ng/ml. Irrespective of TGF-beta1 concentrations, a marked reduction in the stimulatory action of estradiol (10(-9) and 10(-8) M) was observed whereas in combination with tamoxifen (10(-7) and 10(-6) M) only 30 ng/ml TGF-beta1 caused a statistically significant reduction to approximately 30% of the proliferative cells. In further experiments we examined the effect of exposure of breast cancer cells to retinoids in combination with TGF-beta1. The incorporation of [3H]thymidine into MCF-7 cells was inhibited to 52 +/- 19% (control =100%) by 3 ng/ml TGF-beta1, and this dose was used throughout. It was found that addition of TGF-beta1 and isotretinoin to the culture did not decrease proliferation, while TGF-beta1 and tretinoin at low concentrations (3 x 10(-8) and 3 x 10(-7) M) reduced the percentage of proliferating cells by approximately 30% (67+/-8% and 67+/-5%, P
39
Cheng, H., J. G. Yan i Y. Jiang. "Growth suppression of human pancreatic cells by a novel PKCβ inhibitor, enzastaurin". Journal of Clinical Oncology 25, nr 18_suppl (20.06.2007): 14141. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.14141.
Pełny tekst źródłaStreszczenie:
14141 Background: Human pancreatic cancer is a devastating disease. Standard therapy, gemcitabine, is not able to alter the natural history of the disease. Targeting intracellular signaling molecules has proven to be a powerful approach in cancer therapy. Protein kinase C (PKC) family has been implicated in many human cancers including pancreatic cancer. Methods: In this pre-clinical study, we evaluated the effect of a novel small molecule inhibitor, enzastaurin, for PKCβ on human pancreatic cancer cells. We utilized MTT assay to assess cell proliferation and viability. To evaluate cell transforming activity, soft agar colony forming assay was used. Results: We showed that with addition of 20μM enzastaurin into the culture, the proliferative growth of two pancreatic cancer cell lines, Panc1 and L3.6p1, was significantly attenuated, as measured by the MTT assay. In addition, the combination of enzastaurin and a low dose of gemcitabine (25 nM) resulted in a synergistic cytotoxic effect in L3.6p1 cells. Further, the in vitro tumorogenicity assay demonstrated that the L3.6p1 cells treated with enzastaurin (20μM) formed much smaller colonies than the control parental cells in 0.4% soft-agar. Consistent with the in vitro cell proliferation results, the combination of enzastaurin and the low concentration of gemcitabine (25nM) further reduced the numbers and sizes of colonies in the soft-agar. Conclusions: Collectively, our data indicate that enzastaurin can effectively suppress the proliferation and in vitro transforming activity of the pancreatic cells, and more effectively when applied in combination with the low dose of gemcitabine. No significant financial relationships to disclose.
40
Chen, Li-Yu, Gurunath Apte, Annerose Lindenbauer, Marion Frant i Thi-Huong Nguyen. "Effect of HIT Components on the Development of Breast Cancer Cells". Life 11, nr 8 (13.08.2021): 832. http://dx.doi.org/10.3390/life11080832.
Pełny tekst źródłaStreszczenie:
Cancer cells circulating in blood vessels activate platelets, forming a cancer cell encircling platelet cloak which facilitates cancer metastasis. Heparin (H) is frequently used as an anticoagulant in cancer patients but up to 5% of patients have a side effect, heparin-induced thrombocytopenia (HIT) that can be life-threatening. HIT is developed due to a complex interaction among multiple components including heparin, platelet factor 4 (PF4), HIT antibodies, and platelets. However, available information regarding the effect of HIT components on cancers is limited. Here, we investigated the effect of these materials on the mechanical property of breast cancer cells using atomic force microscopy (AFM) while cell spreading was quantified by confocal laser scanning microscopy (CLSM), and cell proliferation rate was determined. Over time, we found a clear effect of each component on cell elasticity and cell spreading. In the absence of platelets, HIT antibodies inhibited cell proliferation but they promoted cell proliferation in the presence of platelets. Our results indicate that HIT complexes influenced the development of breast cancer cells.
41
Dall, Genevieve V., Samuel Hawthorne, Yashar Seyed-Razavi, Jessica Vieusseux, Wanfu Wu, Jan-Ake Gustafsson, David Byrne, Leigh Murphy, Gail P. Risbridger i Kara L. Britt. "Estrogen receptor subtypes dictate the proliferative nature of the mammary gland". Journal of Endocrinology 237, nr 3 (czerwiec 2018): 323–36. http://dx.doi.org/10.1530/joe-17-0582.
Pełny tekst źródłaStreszczenie:
Estrogen induces proliferation of breast epithelial cells and is responsible for breast development at puberty. This tightly regulated control is lost in estrogen-receptor-positive (ER+) breast cancers, which comprise over 70% of all breast cancers. Currently, breast cancer diagnosis and treatment considers only the α isoform of ER; however, there is a second ER, ERβ. Whilst ERα mediates estrogen-driven proliferation of the normal breast in puberty and breast cancers, ERβ has been shown to exert an anti-proliferative effect on the normal breast. It is not known how the expression of each ER (alone or in combination) correlates with the ability of estrogen to induce proliferation in the breast. We assessed the levels of each ER in normal mouse mammary glands subdivided into proliferative and non-proliferative regions. ERα was most abundant in the proliferative regions of younger mice, with ERβ expressed most abundantly in old mice. We correlated this expression profile with function by showing that the ability of estrogen to induce proliferation was reduced in older mice. To show that the ER profile associated with breast cancer risk, we assessed ER expression in parous mice which are known to have a reduced risk of developing ERα breast cancer. ERα expression was significantly decreased yet co-localization analysis revealed ERβ expression increased with parity. Parous mice had less unopposed nuclear ERα expression and increased levels of ERβ. These changes suggest that the nuclear expression of ERs dictates the proliferative nature of the breast and may explain the decreased breast cancer risk with parity.
42
Takeda, Motohiro, Yukina Tanno, Masaki Kobayashi, Balasigamani Devaraj, Masashi Usa i Humio Inaba. "Biophoton emission related with proliferation of cancer cells". JOURNAL OF JAPAN SOCIETY FOR LASER SURGERY AND MEDICINE 16, Supplement (1995): 391–94. http://dx.doi.org/10.2530/jslsm1980.16.supplement_391.
Pełny tekst źródła
43
Hildenbrand, R., M. Gandhari, N. Arens i U. Bleyl. "Urokinase induces proliferation of human breast cancer cells". Pathology - Research and Practice 200, nr 4 (styczeń 2004): 304–5. http://dx.doi.org/10.1016/s0344-0338(04)80591-0.
Pełny tekst źródła
44
Kotake-Nara, Eiichi, Masayo Kushiro, Hong Zhang, Tatsuya Sugawara, Kazuo Miyashita i Akihiko Nagao. "Carotenoids Affect Proliferation of Human Prostate Cancer Cells". Journal of Nutrition 131, nr 12 (1.12.2001): 3303–6. http://dx.doi.org/10.1093/jn/131.12.3303.
Pełny tekst źródła
45
Zhu, Kongxi, Jianqiang Guo, Hongjuan Wang i Weihua Yu. "FRAT1 expression regulates proliferation in colon cancer cells". Oncology Letters 12, nr 6 (19.10.2016): 4761–66. http://dx.doi.org/10.3892/ol.2016.5300.
Pełny tekst źródła
46
Normile, D. "CELL PROLIFERATION: Common Control for Cancer, Stem Cells". Science 298, nr 5600 (6.12.2002): 1869. http://dx.doi.org/10.1126/science.298.5600.1869.
Pełny tekst źródła
47
Chang, Lei, Ruixia Guo i Zhongfu Yuan. "IL-36α suppresses proliferation of ovarian cancer cells". Tumor Biology 39, nr 6 (czerwiec 2017): 101042831770691. http://dx.doi.org/10.1177/1010428317706918.
Pełny tekst źródła
48
Jiang, Xianliang, Ming Li i Li Kei. "MiR-34c regulates the proliferation and apoptosis of lung cancer cells". Clinical and Investigative Medicine 43, nr 4 (27.12.2020): E56–62. http://dx.doi.org/10.25011/cim.v43i4.34997.
Pełny tekst źródłaStreszczenie:
Purpose: As miR-34c acts as a tumor suppressant for multiple cancers, the purpose of this study was to investigate that role that miR-34c plays in the proliferation and apoptosis of lung cancer.
Methods: The expression of miR-34c in 600 patients with lung cancer was quantitatively analyzed with real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) technology and correlated to
clinical pathological parameters. The CCK-8 analysis and flow cytometry were carried out to detect cell proliferation and apoptosis in miR-34c-mimic transfected cell lines. Moreover, the regulation of miR-34c to interleukin-6 (IL-6) in cell lines was detected by western blot, qRT-PCR and dual-luciferase reporter assay.
Results: The expression of miR-34c was downregulated in lung cancer compared with adjacent normal tissues. The expression level of miR-34c was linked to stromal invasion. Furthermore, overexpressing miR-34c played an active role in effectively inhibiting cell proliferation and inducing apoptosis. In addition, a significant inverse relationship was exhibited between the expression of miR-34c and IL-6 in tumor tissues.
Conclusion: At the molecular level, IL-6 can be used as a direct target of miR-34c in the treatment of lung cancer cells and miR-34c can be used as an effective biomarker and therapeutic target for lung cancer.
49
Yang, Mengting, Meng Jin, Kailong Li, Haifeng Liu, Xiaxia Yang, Xiaobei Zhang, Bin Zhang, Aihua Gong i Qingli Bie. "TRAF6 Promotes Gastric Cancer Cell Self-Renewal, Proliferation, and Migration". Stem Cells International 2020 (17.07.2020): 1–11. http://dx.doi.org/10.1155/2020/3296192.
Pełny tekst źródłaStreszczenie:
Gastric cancer is the third most common type of tumor associated with death. TRAF6 belongs to the tumor necrosis factor receptor-associated factor family and has been demonstrated to be involved in tumor progression in various cancers. However, the exact effect of TRAF6 on gastric cancer stem cells has not been extensively studied. In this study, abnormal expression of TRAF6 was found in gastric cancer tissues. Overexpression of TRAF6 enhanced proliferation and migration, and TRAF6 knockdown reversed this phenomenon in gastric cancer cells. Moreover, TRAF6 may inhibit differentiation and promote stemness and epithelial-mesenchymal transition (EMT). Transcriptome profiles revealed 701 differentially expressed genes in the wild-type group and the TRAF6 knockout group. Potential molecules associated with cell proliferation and migration were identified, including MAPK, FOXO, and IL-17. In conclusion, TRAF6 is a significant factor promoting proliferation and migration in gastric cancer cells and may provide a new target for the accurate treatment of gastric cancer.
50
Liang, Zhiyu, i Chuan Li. "Downregulation of miR-24 Enhances Cisplatin Sensitivity in Breast Cancer Cells". Journal of Biomaterials and Tissue Engineering 11, nr 8 (1.08.2021): 1643–48. http://dx.doi.org/10.1166/jbt.2021.2728.
Pełny tekst źródłaStreszczenie:
GSK-3β is a tumor suppressor gene in multiple cancers by phosphorylated degrading β-catenin. Several studies showed association of miR-24 with breast cancer. Bioinformatics analysis showed a relationship of miR-24 with GSK-3β. Our study assessed miR-24’s role in GSK-3β/β-catenin siganling and breast cancer cell cisplatin resistance. MiR-24, GSK-3β, β-catenin, and Bcl-2 expressions in MDA-MB-231 and MDA-MB-231/DDP cells were detected along cell proliferation and apoptosis. DDP resistance cells were assigned into miR-NC, miR-24 inhibitor, pIRES-blank, pIRES-GSK-3β, and miR-24 inhibitor+pIRES-GSK-3β groups and cell proliferation was determined. MiR-24 inhibited GSK-3β level. GSK-3β and cell apoptosis significantly downregulated, while miR-24, β-catenin, Bcl-2, and cell proliferation significantly elevated in DDP resistance cells. MiR-24 inhibitor and/or pIRES-GSK-3β significantly increased GSK-3β level, declined β-catenin and Bcl-2 expressions, attenuated cell proliferation, enhanced cell apoptosis, and weakened cisplatin resistance. MiR-24 upregulation was related to breast cancer cell cisplatin resistance. Inhibition of miR-24 upregulated GSK-3β, restrained Wnt/β-catenin signaling and cisplatin resistance in breast cancer cells.