Academic literature on the topic 'Cancer cell physiology'
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Cancer cell physiology.'
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.
Journal articles on the topic "Cancer cell physiology"
1
Gao, Sumei, Xiaoyan Li, Xia Ding, Wenwen Qi, and Qifeng Yang. "Cepharanthine Induces Autophagy, Apoptosis and Cell Cycle Arrest in Breast Cancer Cells." Cellular Physiology and Biochemistry 41, no. 4 (2017): 1633–48. http://dx.doi.org/10.1159/000471234.
Full textAbstract:
Background: Cepharanthine (CEP) is a biscoclaurine alkaloid extracted from Stephania cepharantha and has been shown to have an anti-tumour effect on different types of cancers. However, the anti-cancer effect of CEP on human breast cancer cells is still unclear. Methods: We used MTT, clone formation, in vitro scratch, invasion and migration assays to confirm the inhibitory role of CEP on the proliferation of breast cancer cells. Flow cytometry, plasmid construction and western blot analysis were used to study the detailed mechanisms. Results: Our study showed that CEP could inhibit cell proliferation by inducing autophagy, apoptosis, and G0/G1 cell cycle arrest of breast cancer cells. Furthermore, we found that CEP induced autophagy and apoptosis by inhibiting the AKT/mTOR signalling pathway. Conclusion: We found that CEP could inhibit growth and motility of MCF-7 and MDA-MB-231 breast cancer cell. Our study revealed an anti-tumour effect of CEP on breast cancer cells and suggests that CEP could be a potential new clinical therapy for breast cancer.
2
Wang, Zhongli, and Chao Liu. "Lgr5-Positive Cells are Cancer-Stem-Cell-Like Cells in Gastric Cancer." Cellular Physiology and Biochemistry 36, no. 6 (2015): 2447–55. http://dx.doi.org/10.1159/000430205.
Full textAbstract:
Background/Aims: Effective treatment of gastric cancer (GC) requires better understanding of the molecular regulation of its carcinogenesis. Identification of cancer stem cells (CSCs) in GC appears to be a critical question. Methods: We analyzed Lgr5 expression in GC specimen. We used an adeno-associated virus (AAV) that carries diphtheria toxin fragment A (DTA) under the control of Lgr5 promoter (AAV-pLgr5-DTA) to transduce human GC cells. The growth of GC cells with/without depletion of Lgr5-positive cells was studied in vitro in an MTT assay, and in vivo by analyzing bioluminescence levels. Results: A portion of GC cells in the resected specimen expressed Lgr5. GC cells that formed tumor spheres expressed high Lgr5. Selective depletion of Lgr5-positive GC cells resulted in significant growth inhibition of GC cells in vitro and in vivo. Conclusion: Lgr5-positive cells may be CSCs-like cells in GC and may play a pivotal role in the tumorigenesis of GC. Treating Lgr5-positive GC cells may substantially improve the therapeutic outcome.
3
Yin, Yu-Chun, Chao-Cheng Lin, Tzu-Ting Chen, Jen-Yeu Chen, Hui-Ju Tsai, Chia-Yu Wang, and Shiow-Yi Chen. "Clozapine Induces Autophagic Cell Death in Non-Small Cell Lung Cancer Cells." Cellular Physiology and Biochemistry 35, no. 3 (2015): 945–56. http://dx.doi.org/10.1159/000369751.
Full textAbstract:
Background/Aims: Previous studies have shown that patients with schizophrenia have a lower incidence of cancer than the general population, and several antipsychotics have been demonstrated to have cytotoxic effects on cancer cells. However, the mechanisms underlying these results remain unclear. The present study aimed to investigate the effect of clozapine, which is often used to treat patients with refractory schizophrenia, on the growth of non-small cell lung carcinoma cell lines and to examine whether autophagy contributes to its effects. Methods: A549 and H1299 cells were treated with clozapine, and cell cytotoxicity, cell cycle and autophagy were then assessed. The autophagy inhibitor bafilomycin A1 and siRNA-targeted Atg7 were used to determine the role of autophagy in the effect of clozapine. Results: Clozapine inhibited A549 and H1299 proliferation and increased p21 and p27 expression levels, leading to cell cycle arrest. Clozapine also induced a high level of autophagy, but not apoptosis, in both cell lines, and the growth inhibitory effect of clozapine was blunted by treatment with the autophagy inhibitor bafilomycin A1 or with an siRNA targeting atg7. Conclusions: Clozapine inhibits cell proliferation by inducing autophagic cell death in two non-small cell lung carcinoma cell lines. These findings may provide insights into the relationship between clozapine use and the lower incidence of lung cancer among patients with schizophrenia.
4
Luo, Hua-Rong, Ying Liu, Xiao-Dong Wan, Jun-Liang Li, Min Wu, Qi-Min Zhang, Deng-Long Wu, Xin Zhao, and Tian-Ru Wang. "Sumoylation Negatively Regulates CSR1-Dependent Prostate Cancer Cell Death." Cellular Physiology and Biochemistry 46, no. 5 (2018): 1861–67. http://dx.doi.org/10.1159/000489370.
Full textAbstract:
Background/Aims: SUMOylation is a dynamic process and reversed by the activity of SUMO-specific proteases (SENPs) family. SENP1, a member of this family, is highly expressed and plays oncogenic roles in diverse cancers including prostate cancer. However, the SENP1-transgenic mice exhibit aberrant transformation of the mouse prostate gland but do not develop cancer. Cellular Stress Response 1 (CSR1) is a tumor suppressor gene and frequently deleted in prostate cancers. Overexpression of CSR1 in prostate cancer cells inhibits colony formation, anchorage-independent growth and induces cell death. Methods: The relationship between CSR1 and SENP1 were determined by immunoprecipitation-based proteomics screen and verified by GST-pull down assay. In vivo SUMOylation assay was used to detect the direct effect of SENP1 in the regulation of CSR1. Clustered regularly interspaced short palindromic repeats (CRISPR)–based gene editing was used to generate Senp1–/– and CSR1–/– PC3 cells. FACS assay was used to determine the apoptosis ratio of cells after transfection. Results: CSR1 is SUMOylated at K582 and rapid ubiquitinated and degradated in prostate cancer cells. SENP1 interacts with and deSUMOylates CSR1 to prevent its degradation and enhances CSR1-dependent prostate cancer cell death. Conclusion: Thus, our data indicates that CSR1 is a critical SUMOylated substrate of SENP1 that might partially explain the controversial roles of SENP1 in prostate cancer development.
5
Cheng, Kunrong, Roxana Samimi, Guofeng Xie, Jasleen Shant, Cinthia Drachenberg, Mark Wade, Richard J. Davis, George Nomikos, and Jean-Pierre Raufman. "Acetylcholine release by human colon cancer cells mediates autocrine stimulation of cell proliferation." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 3 (September 2008): G591—G597. http://dx.doi.org/10.1152/ajpgi.00055.2008.
Full textAbstract:
Most colon cancers overexpress M3 muscarinic receptors (M3R), and post-M3R signaling stimulates human colon cancer cell proliferation. Acetylcholine (ACh), a muscarinic receptor ligand traditionally regarded as a neurotransmitter, may be produced by nonneuronal cells. We hypothesized that ACh release by human colon cancer cells results in autocrine stimulation of proliferation. H508 human colon cancer cells, which have robust M3R expression, were used to examine effects of muscarinic receptor antagonists, acetylcholinesterase inhibitors, and choline transport inhibitors on cell proliferation. A nonselective muscarinic receptor antagonist (atropine), a selective M3R antagonist ( p-fluorohexahydro-sila-difenidol hydrochloride), and a choline transport inhibitor (hemicholinum-3) all inhibited unstimulated H508 colon cancer cell proliferation by ∼40% ( P < 0.005). In contrast, two acetylcholinesterase inhibitors (eserine-hemisulfate and bis-9-amino-1,2,3,4-tetrahydroacridine) increased proliferation by 2.5- and 2-fold, respectively ( P < 0.005). By using quantitative real-time PCR, expression of choline acetyltransferase (ChAT), a critical enzyme for ACh synthesis, was identified in H508, WiDr, and Caco-2 colon cancer cells. By using high-performance liquid chromatography-electrochemical detection, released ACh was detected in H508 and Caco-2 cell culture media. Immunohistochemistry in surgical specimens revealed weak or no cytoplasmic staining for ChAT in normal colon enterocytes ( n = 25) whereas half of colon cancer specimens ( n = 24) exhibited moderate to strong staining ( P < 0.005). We conclude that ACh is an autocrine growth factor in colon cancer. Mechanisms that regulate colon epithelial cell production and release of ACh warrant further investigation.
6
Bose, Shree, Vijyendra Ramesh, and Jason W. Locasale. "Acetate Metabolism in Physiology, Cancer, and Beyond." Trends in Cell Biology 29, no. 9 (September 2019): 695–703. http://dx.doi.org/10.1016/j.tcb.2019.05.005.
Full text
7
Liu, Shunli, Mingrui Chen, Pengcheng Li, Yujia Wu, Chunjuan Chang, Yabin Qiu, Ling Cao, Zhen Liu, and Chiyu Jia. "Ginsenoside Rh2 Inhibits Cancer Stem-Like Cells in Skin Squamous Cell Carcinoma." Cellular Physiology and Biochemistry 36, no. 2 (2015): 499–508. http://dx.doi.org/10.1159/000430115.
Full textAbstract:
Background/Aims: Treatments targeting cancer stem cells (CSCs) are most effective cancer therapy, whereas determination of CSCs is challenging. We have recently reported that Lgr5-positive cells are cancer stem cells (CSCs) in human skin squamous cell carcinoma (SCC). Ginsenoside Rh2 (GRh2) has been shown to significantly inhibit growth of some types of cancers, whereas its effects on the SCC have not been examined. Methods: Here, we transduced human SCC cells with lentivirus carrying GFP reporter under Lgr5 promoter. The transduced SCC cells were treated with different doses of GRh2, and then analyzed cell viability by CCK-8 assay and MTT assay. The effects of GRh2 on Lgr5-positive CSCs were determined by fow cytometry and by tumor sphere formation. Autophagy-associated protein and β-catenin were measured by Western blot. Expression of short hairpin small interfering RNA (shRNA) for Atg7 and β-catenin were used to inhibit autophagy and β-catenin signaling pathway, respectively, as loss-of-function experiments. Results: We found that GRh2 dose-dependently reduced SCC viability, possibly through reduced the number of Lgr5-positive CSCs. GRh2 increased autophagy and reduced β-catenin signaling in SCC cells. Inhibition of autophagy abolished the effects of GRh2 on β-catenin and cell viability, while increasing β-catenin abolished the effects of GRh2 on autophagy and cell viability. Conclusion: Taken together, our data suggest that GRh2 inhibited SCC growth, possibly through reduced the number of Lgr5-positive CSCs. This may be conducted through an interaction between autophagy and β-catenin signaling.
8
Bai, Xiaoxue, Lin Meng, Huijie Sun, Zhuo Li, Xiufang Zhang, and Shucheng Hua. "MicroRNA-196b Inhibits Cell Growth and Metastasis of Lung Cancer Cells by Targeting Runx2." Cellular Physiology and Biochemistry 43, no. 2 (2017): 757–67. http://dx.doi.org/10.1159/000481559.
Full textAbstract:
Background/Aims: Lung cancer is one of the most common causes of cancer related deaths worldwide. The role of several microRNAs (miRNAs) including miR-196b in different cancers has already been established. The study was aimed to explore the role of miR-196b in lung cancer and its possible underlying mechanism. Methods: Human lung cancer cell line A549 was transfected with miR-196b mimic, miR-196b inhibitor and corresponding controls. Then cell viability, migration, invasion, and apoptosis of A549 lung cancer cells either with overexpression or with suppression of miR-196b were estimated sequentially. Next, dual luciferase activity assay was performed to clarify whether Runx2 was a direct target of miR-196b. Finally, the expressions of main factors associated with epithelial mesenchymal transition (EMT), PI3K/AKT/GSK3β, Smad, and JNK pathways were detected by western blot. Results: MiR-196b expression was significantly decreased in A549, H1650 and H1299 cell lines compared with in WI-38 and HEL-1 cell lines. Overexpression of miR-196b suppressed cell viability, migration, invasion, and induced apoptosis as well as inhibited TGF-β induced EMT process in A549 cells. In addition, Runx2 was a putative target of miR-196b, and Runx2 silence remarkably increased cell apoptosis and abolished the promotive effects of miR-196b suppression on cell viability, migration and invasion. Finally, miR-196b also mediated its action by inactivation of PI3K/AKT/GSK3β, Smad, and JNK pathways by down-regulation of Runx2. Conclusion: MiR-196b functions as a tumor suppressor that inhibited cell growth and metastasis of lung cancer cells by targeting Runx2. These findings provided further evidences for treatment of lung cancer.
9
Gao, Zhuo, Ruiqi Liu, Na Ye, Chao Liu, Xiuli Li, Xiaodong Guo, Zhuoran Zhang, Xiaoxi Li, Yuanfei Yao, and Xiaofeng Jiang. "FOXO1 Inhibits Tumor Cell Migration via Regulating Cell Surface Morphology in Non-Small Cell Lung Cancer Cells." Cellular Physiology and Biochemistry 48, no. 1 (2018): 138–48. http://dx.doi.org/10.1159/000491670.
Full textAbstract:
Background/Aims: Cell surface morphology plays pivotal roles in malignant progression and epithelial-mesenchymal transition (EMT). Previous research demonstrated that microvilli play a key role in cell migration of non-small cell lung cancer (NSCLC). In this study, we report that Forkhead box class O1 (FOXO1) is downregulated in human NSCLC and that silencing of FOXO1 is associated with the invasive stage of tumor progression. Methods: The cell proliferation, migration, and invasion were characterized in vitro, and we tested the expression of the Epithelial-mesenchymal transition (EMT) marker by immunofluorescence staining and also identified the effect of FOXO1 on the microvilli by scanning electron microscopy (SEM). Results: Functional analyses revealed that silencing of FOXO1 resulted in an increase in NSCLC cell proliferation, migration, and invasion; whereas overexpression of FOXO1 significantly inhibited the migration and invasive capability of NSCLC cells in vitro. Furthermore, cell morphology imaging showed that FOXO1 maintained the characteristics of epithelial cells. Immunofluorescence staining and western blotting showed that the E-cadherin level was elevated and Vimentin was reduced by FOXO1 overexpression. Conversely, the E-cadherin level was reduced and Vimentin was elevated in cells silenced for FOXO1. Furthermore, scanning electron microscopy (SEM) showed that FOXO1 overexpression increased the length of the microvilli on the cell surface, whereas FOXO1 silencing significantly reduced their length. Conclusions: FOXO1 is involved in human lung carcinogenesis and may serve as a potential therapeutic target in the migration of human lung cancer.
10
Arcangeli, Annarosa, and Jason X. J. Yuan. "American Journal of Physiology-Cell Physiology theme: ion channels and transporters in cancer." American Journal of Physiology-Cell Physiology 301, no. 2 (August 2011): C253—C254. http://dx.doi.org/10.1152/ajpcell.00159.2011.
Full textDissertations / Theses on the topic "Cancer cell physiology"
1
Choi, Mi-Yon. "P53 mediated cell motility in H1299 lung cancer cells." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/109.
Full textAbstract:
Studies have shown that gain-of- function mutant p53, AKT, and NFκB promote invasion and metastasis in tumor cells. Signals transduced by AKT and p53 are integrated via negative feedback between the two pathways. Tumor derived p53 was also indicated to induce NFκB gene expression. Due to the close relationship between p53/AKT and p53/NFκB, we hypothesized that AKT and NFκB can enhance motility in cells expressing mutant p53. Effects on cell motility were determined by scratch assays. CXCL5- chemokine is also known to induce cell motility. We hypothesized that enhanced cell motility by AKT and NFκB is mediated, in part, by CXCL5. CXCL5 expression levels in the presence and absence of inhibitors were determined by qRT-PCR. We also hypothesized that gain-of-function mutant p53 contributes to the activation of AKT. The effect of mutant p53 on AKT phosphorylation was investigated with a Ponasterone A- inducible mutant cell line (H1299/R175H) and vector control. These results indicated that AKT and NFκB enhance motility in cells expressing mutant p53 and this enhanced motility is, in part, mediated by CXCL5. However, AKT phosphorylation was independent of mutant p53.
2
Levitt, Randy J. "Aspects of insulin-like growth factor physiology in cancer." Thesis, McGill University, 2006. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111826.
Full textAbstract:
The insulin-like growth factor (IGF) pathway consists of two ligands (IGF-I and IGF-II), two receptors (IGF-IR and IGF-IIR) and six IGF binding proteins (IGFBP-I through -6). There is considerable evidence from both laboratory and population studies that IGF physiology is relevant to neoplastic growth. For example, it has been shown that IGF-I and/or IGF-II act as mitogens and anti-apoptotic agents for both normal and malignant cells by binding to the IGF-IR and activating downstream signalling pathways. Consistent with this data, IGF-IR inhibition by a variety of strategies inhibits cancer cell proliferation and/or induces apoptosis both in vitro and in animal models of neoplasia. Furthermore, epidemiological studies have demonstrated a positive correlation between serum IGF-I levels and risk of subsequent cancer. Classically, the IGFBPs were considered to be growth inhibitors, as they had a well-defined role in sequestering the mitogens IGF-I and IGF-II, therefore preventing binding and subsequent activation of mitogenic and anti-apoptotic pathways downstream of the IGF-IR. However, increasing evidence indicates that under certain conditions, IGFBPs can act as growth stimulators, and both IGF-dependent and -independent mechanisms have been proposed.Although the roles of the IGFs, IGF-IR and IGFBPs in cancer have been studied extensively, this thesis describes several new links between IGF physiology and neoplasia. In the first section, we demonstrate that IGF-I can attenuate growth inhibition and apoptosis induced by a class of drugs called COX-2 inhibitors in BxPC-3 pancreatic cancer cells. This effect could be attributed to opposite influences of IGF-IR signalling and COX-2 inhibitors on activation of Akt, with IGF-IR signalling increasing activity and COX-2 inhibitors decreasing activity. In the second section, we demonstrate that in 184htert cells, an immortal but untransformed breast epithelial cell line, COX-2 inhibitors can induce IGFBP-3 expression. We go on to show that IGFBP-3 can inhibit growth of this cell line in an IGF-dependent manner, and speculate that this action of COX-2 inhibitors may be relevant to data linking use of this class of drugs to decreased breast cancer risk. In the third section, we demonstrate that the expression of IGFBP-2 in U251 glioma cells is inhibited by the induction of the tumor suppressor PTEN. Furthermore, IGFBP-2 does not effect the growth of this cell line, indicating that published associations between tumor IGFBP-2 expression and grade of glioma may be a result of IGFBP-2 acting as a marker for loss of function of PTEN. In the fourth and final section, we demonstrate that in MDA-MB-231 breast cancer cells, over-expression of IGFBP-2 can enhance growth, indicating that the effect of IGFBP-2 on growth of neoplastic cells is tissue specific. Furthermore, antisense strategies targeting IGFBP-2 mRNA (antisense oligonucleotides and siRNA) can inhibit growth of IGFBP-2-expressing breast cancer cells both in vitro and in vivo.
Taken together, these results extend the existing body of evidence demonstrating that IGF physiology contributes to neoplastic growth, and suggest that strategies to inhibit IGF-IR signalling and/or IGFBP-2 expression may have therapeutic value for some types of cancers.
3
Tang, Haoran. "Scar/WAVE complex suppresses cell invasion and cancer cell transformation." Thesis, University of Glasgow, 2012. http://theses.gla.ac.uk/3633/.
Full textAbstract:
The mechanisms by which cancer cells hijack the actin cytoskeleton to invade and disseminate to distant sites of metastasis remains one of the great frontiers in cancer research. Many actin-regulating proteins have been identified to be important in cancer cell invasion and metastasis. However the role of a major actin assembly promoting complex, Scar/WAVE regulatory complex (WRC) in cancer cell invasion is poorly understood. WRC has a well-known motility-promoting role in 2D planar cell migration, but a recent study on human epithelial cancers suggests WRC may be anti-invasive in vivo. To investigate the controversy, human epithelial cancer cells with reduced WRC expression were tested in multiple 3D cell motility assays. Interestingly, WRC demonstrates a robust anti-invasive role in these exciting experiments. To understand how loss of WRC promotes invasion, the molecular mechanism is investigated. N-WASP is the other major actin assembly promoting protein. Unlike WRC, N-WASP is interestingly not required for 2D planar cell migration, but is important for motility in 3D. The interplay of the two major actin assembly promoting proteins has not been explored in 3D cell motility. I report here that loss of WRC promotes hyper-activation of focal adhesion kinase that leads to N-WASP accumulation and activation at the invasive front. This chain of events results in enhanced invasion providing a molecular mechanism of WRC’s anti-invasive function.  In addition to this FAK-N-WASP core mechanism, I also identified a novel pro- invasive role of HSPC300 independently of WRC. Loss of WRC possibly releases free HSPC300 that could subsequently interact with and regulate N-WASP activation during invasion providing a potential direct molecular link between the two proteins. Furthermore, WRC also supresses focal adhesion kinase mediated cell transformation and tumour formation in vivo. In this thesis I therefore demonstrate novel anti-invasion and anti-tumourigenesis functions of WRC. I also show how a novel WRC binding protein, NHS, could negatively regulate WRC function.
4
Behmoaram, Emy. "Biological studies of fascin function in cancer cell invasion and cancer progression." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111596.
Full textAbstract:
The process of metastasis is initiated through the acquisition of inherent and autonomous motile and invasive properties by tumor cells. These phenomena are initiated through a balance between forward cancer cell membrane protrusion and tail retraction, and occur via cell cytoskeleton remodeling, actin reorganization, and coordinated focal adhesion assembly and disassembly events. Among the vast network of cytoskeletal proteins, the actin-bundling protein fascin plays a major function in cell cytoskeleton remodeling. It is a 55-kDa protein involved in the formation of filopodia and cell migration, and found to be upregulated in many cancers. We report herein key functions for fascin in the regulation of prostate and breast cancer progression. Fascin expression is upregulated in localized and hormone refractory prostate cancer, responsible for a more aggressive clinical course. In addition, functional dissection of fascin reveals a novel function in the regulation of focal adhesion turnover dynamics, by modulating the phosphorylation state of central focal adhesion proteins through a potential collaboration with the protein tyrosine phosphatase, PEST. Together, our data support the importance of fascin in cancer cell invasion and as a significant prognostic marker and a potential therapeutic target for aggressive cancers.
5
Guerrini, Giuditta, and Fabio Carraro. "Hedgehog signalling pathway and Carbonic Anhydrases in Breast cancer cell physiology." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1071510.
Full textAbstract:
Breast cancer (BC) is one of the most diffused types of cancer worldwide. It affects predominantly women and is a highly curable disease if diagnosed at early stage. Several classifications of BC do exist according to different histopathological and molecular features. The worst subtype of BC are triple negative breast cancers (TNBCs) that do not express Estrogen (ER), Progesterone (PgR) and epidermal growth factor 2 (HER2) receptors consequently, these tumors are not sensitive to hormonal therapy. Nowadays, there is no specific clinical guideline approved, therefore, TNBCs treatment consists of cytotoxic agents and radiotherapy. The Hedgehog (Hh) pathway plays a pivotal role during the development of the organism and its expression is tightly controlled and normally kept silent in adult tissue. The Hh pathway indeed is reactivated for homeostasis maintenance after tissue injury or for the physiological tissue renewal. Deregulation of the Hh pathway is associated with development disturbs, underlining the relevance of its precise controlled expression. More and more Hh signalling is found to be involved in cancer development and progression. A growing body of literature underlines the correlation between the Hh pathway and bad prognosis for BCs. Indeed, the Hh pathway is normally silenced in normal breast epithelium and aberrantly activated in TNBCs, where it is associated with a more aggressive phenotype, enhancing proliferation, migration and invasion, furthermore, its activation is related to chemoresistant phenotypes of TNBCs. Carbonic anhydrases (CAs) are evolutionary conserved enzymes, mostly known for their role in pH regulation. CAs catalyze the reversible hydration of H2CO3 into CO2 and H2O. Several other roles have been described and attributed to CAs, from cell survival and migration, to the priming of the stem cell niche. Several CAs classes have been characterized and are conserved among the species. The classification is done according to the subcellular localization of CAs. Membrane bound CAs namely CAIX and CAXII, are overexpressed and active in cancer. While the role of CAIX is associated to bad prognosis, the role of CAXII has a contradictory outcome and still need to be elucidated. In BC, downregulation of CAXII reduced MDAMB231 cell migration through a reduction in p38 phosphorylation, while some researchers confer to the presence of this protein, a good prognostic value. We demonstrate for the first time a correlation between the Hh pathway and CAXII in controlling BCs pathology, emphasising how the activation of the Hh pathway is crucial in the control of CAXII expression, with consistent effects on cell proliferation, migration and invasion. Understanding the reciprocal regulation could be of main interest and should be taken into account in the design of new molecules to improve BC patient’s life expectancy.
6
Scott, Hannah Elizabeth. "PKC-δ, its C2 domain and breast cancer cell lines." Thesis, University of Nottingham, 2012. http://eprints.nottingham.ac.uk/12668/.
Full textAbstract:
Protein kinase C δ (PKC-δ) is a novel member of the PKC family of serine-threonine kinases. PKC-δ structure is widely conserved within the PKC family and has a catalytic region and regulatory region. The regulatory region has two main sub domains C1 and C2. Although several studies have investigated the role of the C1 domain, little is known about the function of the C2 domain, however there is some evidence that it acts as a protein interaction domain. PKCs are involved in a wide variety of cellular functions within cancer. PKC-δ has been demonstrated to have a particular involvement with the apoptotic processes of a cancer cell. A pro-apoptotic role for PKC-δ has been identified, whereby tyrosine phosphorylation of particular residues induces translocation to the nucleus, alongside a similar translocation event for caspase-3. In the nucleus, caspase-3 cleaves the regulatory and catalytic regions to form a free catalytic domain that is uninhibited by the regulatory portion. This free catalytic region causes the induction of the apoptotic pathway. Conversely an anti-apoptotic role has also been identified for PKC-δ. This was found in MDA-MB-231 cells, which have a ras mutation. Due to this mutation in these cells, ERK1/2 phosphorylation is high. Without PKC-δ activity the high phosphorylation levels induce apoptosis. PKC-δ acts on a pathway to reduce ERK1/2 phosphorylation, thus facilitating cell survival. This study aimed to investigate the role of the PKC-δ C2 domain within breast cancer cells. Through use of these techniques, the role of the C2 domain was examined in order to consider its utility as a drug target to treat breast cancer. •Constructs were developed of pIRESneo2 vector with myc-tagged C2 domain and myc-tagged PKC-δ sequences •Breast cancer cell lines, MDA-MB-468, MDA-MB-231 and MCF-7, were stably transfected with a vector control and myc-δC2 construct. MDA-MB-231 and MCF-7 were also transfected with myc-PKC-δ. •Cell lines developed were examined for alterations due to the presence of the C2 domain or PKC-δ over-expression As the C2 domain is proposed to be a protein interaction domain, we hypothesized that over-expression of this domain would interfere with endogenous PKC-δ interactions, through competitive inhibition, and thus we could identify C2 domain roles. The effect on the cells of the endogenous PKC-δ would be opposed by the C2 domain. Thus the role of endogenous PKC-δ could also be clarified for a particular situation - it would be the opposite of the effects induced by the myc-δC2 on the cells. In the MDA-MB-468 stable cell lines, immuno-fluorescence examination of the myc-δC2 cells showed the myc-δC2 was localised at the ends of actin protrusions from the bulk of the cell. The myc-δC2 expressing cells had a more extensive cytoskeleton than the Vector control cells, possibly suggesting improved attachment to a surface. An experiment examining this illustrated that the myc-δC2 cells appeared to attach in a shorter time period. This implies that the role of the endogenous PKC-δ is to discourage cell attachment and promote an invasive phenotype, this is in agreement with the literature. During sub-culture of the MDA-MB-468 cell lines it became apparent that the myc-δC2 cells were growing at an increased rate over the Vector cell lines. This was quantified and indeed the myc-δC2 cells did increase in cell number more than the Vector cells. This was also the case with the MDA-MB-231 cells but not with the MCF-7 cells. Growth is a balance of proliferation and apoptosis. This effect indicates that PKC-δ is pro-apoptotic, or anti-proliferative. MCF-7 cells lack caspase-3 and thus pro-apoptotic effects of PKC-δ would be affected in this cell line. As the myc-δC2 did not have an effect in these cells we examined apoptosis to see if these effects could be attributed to differences in apoptosis. The MDA-MB-468 cells expressing myc-δC2 had higher viability than the Vector cells. This fits with the cell number data, indicating that a lower level of apoptosis has led to a greater cell number, and advocates a pro-apoptotic role for PKC-δ. This was not the case in MDA-MB-231 cell lines where Vector cells had higher viability. This agrees with the literature describing PKC-δ displaying an anti-apoptotic role in this cell line, but does not fit with the cell number data. Thus, differences in cell number are likely due to effects on proliferation, although this was not investigated. MCF-7 cells showed no differences indicating the apoptotic program of these cells is indeed affected by the lack of caspase-3. Serum starvation is a commonly used method to induce apoptosis. MDA-MB-468 cell lines were serum starved in order to examine the effects. The apoptosis profile was altered and myc-δC2 cells showed lower viability than the Vector cells, indicative of an anti-apoptotic effect of PKC-δ. An anti-apoptotic effect is observed in MDA-MB-231 cells, where the effect was proteasome dependent. This was also the case in this situation. The anti-apoptotic effect is related to levels of phosphorylated ERK1/2, where high levels are pro-apoptotic. The phosphorylation status was examined and illustrated a much higher level of phosphorylation in myc-δC2 cells over Vector cells when starved. This indicates myc-δC2 is inhibiting the de-phosphorylating role of PKC-δ in these apoptotic cells. Thus it appears that the C2 domain acts as a ‘sensor’ to serum status, appropriating PKC-δ effects in apoptotic pathways according to the serum status, the method of which is unknown. This study has highlighted the importance of the PKC-δ C2 domain in breast cancer apoptosis. The effects appear to require a fully active PKC-δ pro-apoptotic pathway, and are dependent on the serum status of the cells. Further investigation would be required to identify a level of serum for use in vitro that is relevant to an in vivo tumour situation. If low levels are more relevant to a clinical state then it may be possible to target the C2 domain with drugs to allow induction of apoptosis. The differences between the cell lines clearly show that the phenotypic analysis of tumours would be vital to identifying whether such treatment would be applicable, as effects of any drug would vary greatly across tumour types. MDA-MB-468 and MDA-MB-231 are both triple negative cell lines (i.e. they do not express progesterone, oestrogen or HER2 receptors); however the strong differences seen in this case indicate further phenotypic analysis would be essential.
7
Kumar, Jothi Dinesh. "Novel stromal cell signalling systems in oesophageal cancer." Thesis, University of Liverpool, 2013. http://livrepository.liverpool.ac.uk/15257/.
Full textAbstract:
Myofibroblasts are recognised to play an important role in wound healing and the maintenance of tissue integrity. In addition, they are increasingly recognised to provide a supporting microenvironment for cancer cells. They secrete a variety of chemokines, cytokines, growth factors and proteases that collectively regulate cell proliferation, migration and invasion. Specific chemokines are known to recruit mesenchymal stromal cells (MSCs) to both tumours and normal tissue which may then give rise to myofibroblasts. Proteomic studies by Holmberg and Varro (unpublished observations) identified chemerin as an upregulated chemokine in conditioned media (CM) from oesophageal cancer associated myofibroblasts (CAMs) compared to adjacent tissue myofibroblasts (ATMs). Chemerin is potent chemo-attractant for immune and inflammatory cells. The objectives of this thesis were (a) to functionally characterise the oesophageal myofibroblasts,(b) validate the findings of previous proteomic studies and (c) determine the role of chemerin in MSC migration. Oesophageal CAMs from both squamous and adenocarcinoma tumours were shown to be more proliferative than their paired ATMs, or normal tissue myofibroblasts (NTMs). In addition, CAM conditioned media increased the proliferation and migration of two oesophageal cancer cell lines (OE21 and OE33) and stimulated MSC migration compared to ATM CM. The data suggest oesophageal CAMs promote an aggressive tumour microenvironment. Western blotting and ELISA confirmed increased chemerin secretion by squamous carcinoma CAMs. Chemerin and conditioned media from squamous carcinoma CAMs, stimulated MSC and OE21 cell migration; Chemerin neutralizing antibody reversed these effects and siRNA knockdown of chemerin in CAMs, or of its cognate receptor ChemR23 in MSCs, decreased migratory responses. Studies using pharmacological inhibitors or Western blot of cellular proteins indicated that chemerin stimulated MSCs via PKC, and p42/44, p38 MAP and JNK kinases. Macrophage Inhibitory Factor (MIF) was identified as a putative chemerin target in MSCs and validated by ELISA and Western blot of MSC media and cell extracts. MIF inhibited MSC migration in response to low or moderate concentrations of chemerin, indicating that it might restrain MSC migration in normal tissues but not in cancers where chemerin is elevated. Finally, confirmation of chemerin-chemR23 interactions was obtained using a chemR23 antagonist, CCX832. Chemerin induced MSC and OE21 cell migration was inhibited by CCX832. Moreover, transendothelial migration of MSCs in response to chemerin or CAM conditioned media was reversed by CCX832. Transendothelial migration was also shown to depend on chemerin-stimulated MMP-2 secretion. These findings indicate a molecular mechanism by which MSCs are recruited to tumours. Taken as a whole, this work indicates that myofibroblasts derived from oesophageal cancers differ from those in adjacent or normal tissue. The finding of increased chemerin in these cells is novel and may be relevant to MSC recruitment. Since it is possible to inhibit the effects of chemerin on MSCs using CCX832, there is the potential for a novel therapeutic approach to prevent cancer progression.
8
Swanson, Tara. "Physiological correlates of cancer-related fatigue in advanced non-small cell lung cancer patients." Thesis, McGill University, 2005. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=98503.
Full textAbstract:
Background. Fatigue is a debilitating consequence of lung cancer and its treatments. Reviewing the literature in cancer-related fatigue provides few etiological factors, making evidence-based interventions limited. In this study, previously identified factors as well as muscular and cardiorespiratory function were assessed as potential contributors to fatigue in stages 3A/B and 4 NSCLC patients.Methods. Participants were evaluated by a physical therapist within the McGill Cancer Nutrition and Rehabilitation Program. Performance-based measures of physical function [upper limb strength and endurance (Jamar dynamometry), lower limb strength (30sec chair rise), cardiorespiratory function (2 minute walk - 2MW)] and a symptom questionnaire (Edmonton Symptom Assessment Scale) were conducted at one point in time. The primary endpoint of global fatigue rating was assessed using the Brief Fatigue Inventory (BFI).
Results. Fifty-eight patients (30M:28F, mean age 68 +/- 12) participated in the study. Forty-three percent were actively receiving treatment at the time of assessment. On the BFI, 67% had moderate or severe fatigue and 84% indicated fatigue had interfered with their functioning during the past 24 hours. Global fatigue scores were unrelated to hand grip strength or endurance measurements, hematological parameters or sleep quality but were significantly correlated with chair rise performance, overall rating of breathlessness, patient rating of pain and patient rated weakness. Multivariate regression analysis suggested the best model for global fatigue scores incorporates patients' ratings of weakness, breathlessness and chair rise performance.
Conclusions. Fatigue is prevalent and impacts on the function of advanced NSCLC patients. Several key factors contribute to this fatigue, with muscular and cardiorespiratory restrictions playing an important role. Such findings may have clinical implications in the recommendations of rest and exercise to best manage fatigue.
9
Christofakis, Emil Paul. "Effects of CXCL8 Overexpression on Tumor Cell Proliferation and Migration in an HNSCC Cell Model." VCU Scholars Compass, 2007. http://scholarscompass.vcu.edu/etd/1475.
Full textAbstract:
Head and neck squamous cell carcinoma is the 6th most common malignancyworldwide. Recently, a link between cancer and inflammation has been found. Mediatingthis relationship are the chemotactic cytokines known as chemokines. CXCL8 (Interleukin-8), a CXC ELR+ Chemokine mainly responsible for neutrophil chemoattraction, has beenimplicated in increased tumor proliferation, migration and angiogenesis. The current studytests the effects of CXCL8 on the tumor proliferation and metastasis. By genetically modifying cells to knockdown or overexpress the CXCL8 gene we tested its biological rolein head and neck cancer progression. Overexpression of CXCL8 in HN4 tumor cells withlow endogenous CXCL8 levels was found to increase tumor growth, as judged by cellcounting and MTT assays. Conversely, RNAi-mediated knockdown of CXCL8 expressionin HN12 cells, which express high levels of this chemokine, resulted in a decrease inproliferation. Similarly, overexpression of CXCL8 enhanced migration of HN4 cells invitro, while knockdown inhibited HN12 cell migration and invasion through a basementmembrane substitute. Taken together, these findings support the hypothesis that CXCL8affects multiple processes involved in head and neck cancer tumor progression. The datasuggest that CXCL8 is a potential therapeutic target for head and neck, and other, cancers.
10
Thomas, Mark Peter. "Differential tolerance of a cancer and a non-cancer cell line to amino acid deprivation : mechanistic insight and clinical potential." Thesis, Stellenbosch : Stellenbosch University, 2012. http://hdl.handle.net/10019.1/19912.
Full textAbstract:
Thesis (PhD)--Stellenbosch University, 2012.ENGLISH ABSTRACT: Introduction – Due to spatial separation from the native vascular bed, solid tumours develop regions with limited access to nutrients essential for growth and survival. The promotion of a process known as macroautophagy may facilitate in the maintenance of intracellular amino acid levels, through breakdown of cytoplasmic proteins, so that they remain available for macromolecular biosynthesis and ATP production. Several studies point to the potential ability of some cancers to temporarily increase autophagy and thereby prolong cell survival during metabolic stress. The validity of these claims is assessed when a commonly used breast cancer cell line and an epithelial breast cell line are starved of amino acids in this study. Furthermore, we go on to hypothesize that acute amino acid deprivation during treatment will result in an elevated sensitivity of MDAMB231 cells to doxorubicin toxicity but limit its cytotoxic side-effects in MCF12A cells. Methods and study design- Human breast cancer cells (MDAMB231) and breast epithelial cells (MCF12A) cultured in complete growth medium were compared to those incubated in medium containing no amino acids. Steady state autophagy levels were monitored using classical protein markers of autophagy (LC3-II and beclin-1) and the acidic compartmentalization in cells (Lysotracker™ red dye) in conjunction with autophagy inhibition (bafilomycin A1 and ATG5 siRNA). Cell viability was monitored using several techniques, including caspase 3/7 activity. ATP levels were assessed using a bioluminescent assay, while mass spectrometry based proteomics was used to quantify cellular amino acid levels. Similar techniques were used to monitor autophagy during doxorubicin treatment, while cellular doxorubicin localization was monitored using immunofluorescence microscopy. Finally, a completely novel GFP-LC3 mouse tumour model was designed to assess autophagy and caspase activity within tumours in vivo, during protein limitation and doxorubicin treatment. Results - Amino acid deprivation resulted in a transient increase in autophagy at approximately 6 hours of amino acid starvation in MDAMB231 cells. The amino acid content was preserved within these cells in an autophagy-dependent manner, a phenomenon that correlated with the maintenance of ATP levels. Inhibition of autophagy during these conditions resulted in decreased amino acid and ATP levels and increased signs of cell death. MCF12A cells displayed a greater tolerance to amino acid starvation during 24 hours of amino acid starvation. Evidence indicated that autophagy was important for the maintenance of amino acid and ATP levels in these cells and helped prevent starvation-induced cell death. Furthermore, data showed that concomitant amino acid withdrawal resulted in decreased cellular acidity in MDAMB231 cells, and increased acidity in MCF12A cells, during doxorubicin treatment. These changes correlated with evidence of increased cell death in MDAMB231 cells, but a relative protection in MCF12A cells. A novel model was used to apply these techniques in vivo, and although mice fed on a low protein diet during high dose doxorubicin treatment had increased mean survival and smaller tumour sizes, evidence suggested that autophagy is protecting a population of cells within these tumours. Conclusions - This novel approach to tumour sensitization could have several implications in the context of cancer therapy, and given the delicate relationship that autophagy has with the cancer microenvironment, efforts to determine the mechanisms involved in autophagy and sensitization could lead to new and innovative treatment opportunities for cancer management.
AFRIKAANSE OPSOMMING: Inleiding – As gevolg van hul skeiding van die oorpronklike vaskulêre netwerk, ontwikkel soliede gewasse areas met beperkte toegang tot noodsaaklike voedingstowwe. Die bevordering van 'n proses wat as makro-autofagie bekend staan, kan die handhawing van intrasellulêre aminosuur vlakke fasiliteer. Voorafgenoemde proses word waarskynlik deur die afbreek van sitoplasmiese proteïene teweegebring om sodoende vir makro-molekulêre biosintese en ATP produksie beskikbaar te kan wees. Verskeie studies dui daarop dat sommige kankersoorte die vermoë het om autofagie tydelik te verhoog, en daarby sel oorlewing gedurende metaboliese stress te verleng. Die geldigheid van hierdie eise word evalueer wanneer 'n algemeen beskikbare borskanker sellyn, en 'n borsepiteelsellyn in hierdie studie van aminosure verhonger word. Verder, veronderstel ons dat akute aminosuur ontneming gedurende behandeling 'n verhoogde sensitiwiteit van MDAMB231 selle tot doxorubicin toksisiteit tot gevolg sal hê, maar terselfdetyd die middel se sitotoksiese newe-effekte in MCF12A selle sal beperk. Metodes en studie ontwerp – Menslike borskanker- (MDAMB231) en bors epiteel selle (MCF12A) wat in volledige groeimedium gekweek is, is vergelyk met selle wat in aminosuur vrye medium gekweek is. Basislyn autofagie-vlakke is gemonitor deur die gebruik van klassieke autofagie proteïen merkers (LC3-II en beclin-1) en die asidiese kompartementalisering in selle (Lysotracker™ rooi kleurstof) saam met autofagie inhibisie (bafilomycin A1 and ATG5 siRNA). Sellewensvatbaarheid is deur die gebruik van verskeie tegnieke, insluitend caspase 3/7 aktiwiteit, gemonitor. ATP-vlakke is deur die gebruik van 'n bioluminiserende tegniek gemeet, terwyl massa-spektrometrie-gebaseerde “proteomics” gebruik is om sel aminosuur vlakke te kwantifiseer. Soortgelyke tegnieke is gebruik om autofagie gedurende doxorubicin behandeling waar te neem, terwyl sellulêre doxorubicin lokalisasie deur die gebruik van immunofluoresensie mikroskopie gemonitor is. Ten slotte, is 'n unieke GFP-LC3 muismodel in hierdie studie ontwikkel. Hierdie model is gebruik om autofagie en caspase aktiwiteit in gewasse in vivo te bestudeer tydens proteïen beperking en doxorubicin behandeling. Resultate – Aminosuur ontneming het tot 'n tydelike verhoging in autofagie na ongeveer 6 ure van aminosuur verhongering in MDAMB231 selle gelei. Die aminosuur inhoud van hierdie selle het op 'n autofagie-afhanklike manier behoue gebly. Hierdie verskynsel het met die handhawing van ATP-vlakke gekorreleer. Autofagie inhibisie gedurende hierdie kondisies het 'n verlaging in aminosuur en ATP-vlakke teweeggebring, sowel as vermeerderde tekens van seldood tot gevolg gehad. MCF12A selle het 'n groter toleransie tot aminosuur verhongering tydens die 24 uur aminosuur verhongeringsperiode getoon. Getuienis het aangedui dat autofagie belangrik vir die handhawing van aminosuur en ATP-vlakke in hierdie selle was, en gehelp het om verhongerings-geïnduseerde seldood te voorkom. Verder het data gewys dat aminosuur ontrekking tot verminderde sellulêre asiditeit in MDAMB231 selle, en verhoogde asiditeit in MCF12A selle gedurende doxorubicin behandeling gelei het. Hierdie veranderinge stem ooreen met getuienis van toenemende seldood in MDAMB231 selle, maar 'n relatiewe beskerming in MCF12A selle. 'n Unieke model was gebruik om hierdie tegnieke in vivo toe te pas. Alhoewel verhoogde oorlewing en kleiner gewasse in muise op 'n lae proteïen dieet gedurende hoë dosis doxorubicin behandeling opgemerk is, het bewyse voorgestel dat autofagie 'n populasie selle binne die gewasse beskerm. Gevolgtrekkings – Hierdie unieke benadering tot tumor sensitisering kan verskeie implikasies in die konteks van kanker behandeling hê. Gegewe die delikate verhouding van autofagie met die kanker mikro-omgewing, kan pogings om die meganismes betrokke in autofagie en sensitisering te bepaal, tot nuwe en innoverende behandelings vir kanker lei.
Books on the topic "Cancer cell physiology"
1
W, Masters John R., and Palsson Bernhard, eds. Cancer cell lines. Dordrecht: Kluwer Academic Publishers, 1999.
Find full text
2
Harvey, Amanda. Cancer cell signalling. Chichester, West Sussex: John Wiley & Sons, Inc., 2013.
Find full text
3
-Y, Wang J., and Casero Robert Anthony, eds. Polyamine cell signaling: Physiology, pharmacology, and cancer research. Totowa, N.J: Humana Press, 2006.
Find full text
4
Avner, Friedman, and Aguda B, eds. Cell cycle, proliferation, and cancer. Berlin: Springer, 2006.
Find full text
5
Malcolm, Steinberg, ed. The Cell surface in development and cancer. New York: Plenum Press, 1986.
Find full text
6
Mirzayans, Razmik. Cellular senescence: Implications for cancer therapy. New York: Nova Biomedical Books, 2009.
Find full text
7
S, Stein Gary, and Pardee Arthur B. 1921-, eds. Cell cycle and growth control: Biomolecular regulation and cancer. 2nd ed. Hoboken, NJ: Wiley-Liss, 2004.
Find full text
8
1939-, Wilson Samuel H., and Hoagland Mahlon B, eds. Cancer biology and biosynthesis. Boca Raton, Fla: CRC Press, 1991.
Find full text
9
Calcium, cell cycles, and cancer. Boca Raton, Fla: CRC Press, 1990.
Find full text
10
service), ScienceDirect (Online, ed. Programmed cell death: General principles for studying cell death. San Diego, Calif: Academic Press, 2008.
Find full textBook chapters on the topic "Cancer cell physiology"
1
Wang, Ji Ming, Weipin Shen, Oleg Chertov, Jo Van Damme, and Joost J. Oppenheim. "Chemokine Modulation of Tumor Cell Physiology." In Chemokines and Cancer, 129–41. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-701-7_8.
Full text
2
Kampa, M., A. P. Nifli, G. Notas, and E. Castanas. "Polyphenols and cancer cell growth." In Reviews of Physiology, Biochemistry and Pharmacology, 79–113. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/112_2006_0702.
Full text
3
Bissell, Mina J. "The Central Role of Basement Membrane in Functional Differentiation, Apoptosis, and Cancer." In Cell Death in Reproductive Physiology, 125–40. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-1944-6_12.
Full text
4
Gaudino, G., L. Gandino, M. Cilli, A. Mondino, and P. M. Comoglio. "The Bombesin Receptor Complex and Cell Growth: Physiology and Pathology." In New Concepts in Cancer, 196–207. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-10671-4_14.
Full text
5
Molino, Natalie, K. Ververis, and Tom C. Karagiannis. "Principles of the Warburg Effect and Cancer Cell Metabolism." In Molecular mechanisms and physiology of disease, 355–69. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0706-9_12.
Full text
6
Sidler, F., T. Wermelinger, L. Rist, A. Hensel, and A. Viviani. "Influence of Mistletoe Extracts and Its Components on in Vitro Physiology of Cancer Cells." In Animal Cell Technology Meets Genomics, 183–85. Dordrecht: Springer Netherlands, 2005. http://dx.doi.org/10.1007/1-4020-3103-3_36.
Full text
7
Tenniswood, Martin, Sean Guenette, Colm Morrissey, Jacintha O’Sullivan, Zhengqi Wang, Ping Zhan, Srikala Sridhar, Johnathon Lakins, and Hailun Tang. "Apoptosis and Tumor Invasion in Hormone-Dependent Cancers." In Cell Death in Reproductive Physiology, 208–29. New York, NY: Springer New York, 1997. http://dx.doi.org/10.1007/978-1-4612-1944-6_17.
Full text
8
Nguyen, David H. "Cellular Plasticity, Cancer Stem Cells, and Cells-of-Origin." In Systems Biology of Tumor Physiology, 21–31. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-25601-6_2.
Full text
9
Aviles, Diego, David Warshal, Lauren Krill, and Olga Ostrovsky. "Extracellular Vesicles and Ovarian Cancer." In Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101412.
Full textAbstract:
Extracellular vesicles (EVs) are a varied group of cell-derived, microscopic, fluid-filled pouches released from cells into neighboring microenvironments that are quickly gaining recognition as a potentially powerful tool against epithelial ovarian cancer (EOC). Recent studies show that not only do EVs play an integral part in the development of cancer through intercellular communication, cell survival, and immune modulation but also may assist with early diagnosis and improved treatments. EOC currently has few effective screening options for early detection of this disease; and, therefore, it is detected at an advanced stage where it is more likely to recur, develop chemoresistance, and ultimately become fatal. Newer research has evaluated EVs as biomarkers for early screening and diagnosis and as novel targets for treatment of EOC. Moreover, EVs are possible targets for novel immunomodulatory therapies to directly target cancer cells or make cancer cells more susceptible to other treatment modalities. Therefore, EVs present an exciting, promising approach which may improve clinical outcome for EOC patients.
10
Jain, Sapna, and Manjari Singh. "Engineering of Extracellular Vesicles as Nano Therapy for Breast Cancer." In Physiology. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.101149.
Full textAbstract:
Extracellular vesicles are membrane-derived nanoparticles that represent a novel mechanism of cell-to-cell communication. It is well reported that EVs play a central role in the tumor microenvironment by mediating intercellular signaling among cancer cells. This has resulted in the development of therapeutic strategies targeting various EV signaling pathways in cancer. However, because of their small size and endogenous origin, they have been extensively explored for cancer drug delivery. Hence, owing to their natural ability to mediate intercellular communication, high stability, and low immunogenicity, they have emerged as an attractive platform for cancer treatment. However, limited production and insufficient loading with therapeutic moieties are some of the issues constraining their clinical translation. In this chapter, recent research studies performed in an attempt to develop EVs as cancer biomarkers or drug delivery systems will be discussed. Further, it will also discuss various strategies such as direct and indirect cell surface modification, which can be employed to make EVs successful as cancer therapeutics. Furthermore, it will highlight the current and completed clinical trials using naturally derived EVs as cancer therapeutics.
Conference papers on the topic "Cancer cell physiology"
1
Takayama, Shuichi, Dongeun Huh, Jonathan Song, Wansik Cha, and Yunseok Heo. "Micro- and Nanofluidics for Cell Biology, Cell Therapy, and Cell-Based Drug Testing." In ASME 2009 7th International Conference on Nanochannels, Microchannels, and Minichannels. ASMEDC, 2009. http://dx.doi.org/10.1115/icnmm2009-82151.
Full textAbstract:
Many biological studies, drug screening methods, and cellular therapies require culture and manipulation of living cells outside of their natural environment in the body. The gap between the cellular microenvironment in vivo and in vitro, however, poses challenges for obtaining physiologically relevant responses from cells used in basic biological studies or drug screens and for drawing out the maximum functional potential from cells used therapeutically. One of the reasons for this gap is because the fluidic environment of mammalian cells in vivo is microscale and dynamic whereas typical in vitro cultures are macroscopic and static. This presentation will give an overview of efforts in our laboratory to develop microfluidic systems that enable spatio-temporal control of both the chemical and fluid mechanical environment of cells. The technologies and methods close the physiology gap to provide biological information otherwise unobtainable and to enhance cellular performance in therapeutic applications. Specific biomedical topics that will be discussed include, in vitro fertilization on a chip, microfluidic tissue engineering of small airway injuries, breast cancer metastasis on a chip, electrochemical biosensors, and development of tuneable nanofluidic systems towards applications in single molecule DNA analysis.
2
Marshall, Lauren, Andra Frost, Tim Fee, and Joel Berry. "Assembly and Characterization of 3D, Vascularized Breast Cancer Tissue Mimics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14199.
Full textAbstract:
Drug development platforms such as two-dimensional (2D) in vitro cell culture systems and in vivo animal studies do not accurately predict human in vivo effectiveness of candidate therapeutics [1]. Cell culture systems have limited similarities to primary human cells and tissues as only one cell type is employed and animal studies have a generally limited ability to recapitulate human drug response as different species have differences in metabolism, physiology, and behavior. Mike Leavitt, a former U.S. Secretary of Health and Human Services, has stated that “currently, nine out of ten experimental drugs fail in clinical studies because we cannot accurately predict how they will behave in people based on laboratory and animal studies” [2]. Therefore, this research project is focused on developing an in vitro platform to test candidate therapeutics for more efficacious predictions of human response. We have fabricated a three-dimensional (3D) breast cancer tissue volume containing a vascular network. This vascular network is necessary because current in vitro systems (e.g., rotating bioreactors, suspension of spheroids, and growth on a porous scaffold) are limited in size (1–2 mm) by their absence of micrometer-scale blood flow micro-channels that allow for oxygen and nutrient diffusion into the tissue [4]. The extracellular matrix scaffold has been developed to mimic the native extracellular matrix and includes relevant cell types (e.g., human breast cancer epithelial cells and human breast fibroblasts) along with the prefabricated vascular network (prevascularization). These systems are intended to support long-term growth, recapitulate physiological tissue function, and accurately model response to treatment. It is hypothesized that the development of reproducible tissue volumes will transform breast cancer drug development by providing reliable, cost-effective models that can more accurately predict therapeutic efficacy than current preclinical in vivo and in vitro models.
3
Nagel, Jacquelyn K. S. "Design of a Biologically-Inspired Chemical Sensor." In ASME 2013 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/detc2013-12378.
Full textAbstract:
Sensors are an integral part of many engineered products and systems. Biological inspiration has the potential to improve current sensor designs as well as inspire innovative ones. Mimicking nature offers more than just the observable aspects that conjure up engineering solutions performing similar functions, but also less obvious strategic and sustainable aspects. This paper presents the design of an innovative, biologically-inspired chemical sensor that performs “up-front” processing through mechanical filtering. Functional representation and abstraction were used to place the biological system information in an engineering context, and facilitate the bioinspired design process. Inspiration from the physiology (function) of the guard cell coupled with the morphology (form) and physiology of tropomyosin resulted in multiple concept variants for the chemical sensor. The chemical sensor conceptual designs are provided along with detailed descriptions. Applications of the sensor design include environmental monitoring of harmful gases, and a non-invasive approach to detect illnesses including diabetes, liver disease, and cancer on the breath.
4
Recio Boiles, Alejandro, Matthias Ilmer, Jody Vykoukal, and Eckhard Alt. "Abstract 2934: TRAIL-resistance in pancreatic cancer stem cells can be regulated through JNK pathway inhibition without impacting resident stem cell physiology." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-2934.
Full text
5
Takayama, Shuichi, Yi-Chung Tung, and Bor-Han Chueh. "Biological Micro/Nanofluidics." In ASME 2008 First International Conference on Micro/Nanoscale Heat Transfer. ASMEDC, 2008. http://dx.doi.org/10.1115/mnht2008-52087.
Full textAbstract:
Many biological studies, drug screening methods, and cellular therapies require culture and manipulation of living cells outside of their natural environment in the body. The gap between the cellular microenvironment in vivo and in vitro, however, poses challenges for obtaining physiologically relevant responses from cells used in basic biological studies or drug screens and for drawing out the maximum functional potential from cells used therapeutically. One of the reasons for this gap is because the fluidic environment of mammalian cells in vivo is microscale and dynamic whereas typical in vitro cultures are macroscopic and static. This presentation will give an overview of efforts in our laboratory to develop programmable microfluidic systems that enable spatio-temporal control of both the chemical and fluid mechanical environment of cells. The technologies and methods close the physiology gap to provide biological information otherwise unobtainable and to enhance cellular performance in therapeutic applications. Specific biomedical topics that will be discussed include subcellular signalling in normal and cancer cells, in vitro fertilization on a chip, studies of the effect of physiological and pathological fluid mechanical stresses on endothelial and epithelial cells, and microfluidic stem cell engineering. In the nanoscale regime, tunable nanochannels that can manipulate single DNA molecules will be discussed.
6
Filippi, J. F., D. Arnoux, N. Tubiana, B. Boutière, F. Le Caär, J. Sampol, Lab Hématol, Pr J. Sampol, and Pr Y. Carcassonne. "PLASMINOGEN ACTIVATOR ACTIVITY OF NORMAL AND MALIGNANT MONONUCLEAR HUMAN CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643167.
Full textAbstract:
Plasminogen activators (PA) are thought to play a role in the invasive and metastatic properties of many types of cancer cells. Though, discrepancies in correlations between fibrinolytic activity and metastatic potential of malignant cells have been described.In this study, we evaluated both tissue type (tPA) and urokinase type (UK) cellular PA activities in different mononuclear cell types : normal T and B human peripheral lymphocytes, B cells from patients with chronic lymphocytic leukemia (CLL), human blood monocytes, alveolar macrophages, U 937, RAJI and JM cell 1ines.Mononuclear cells were isolated by Ficoll-hypaque gradients and monocytes by plastic adhesion. T and B cells were separated by a rosetting technique using sheep red blood cells. Cellular extracts were prepared by 0.5 % Triton X 100 buffer treatment followed by sonication and centrifugation 10 ' at 2000 g. PA assays were performed on the supernatants.UK-type PA was evaluated by a liquid-phase assay in presence of human plasminogen (Kabi) and chromogenic substrate S 2251 (Kabi).tPA was determinated using a solid-phase fibrin activity assay which involves an affinity separation step and thus allows selective detection of tPA.In both cases, results were reported in international units by reference to standard curves of UK (Choay) or tPA (Kabi).In all cell types tested, PA detected was essentially urokinase-type. Highest PA activity was found in U 937 cells (0.7 IU/5×l06 cells). In normal blood lymphocytes, mean PA activity was 0.08 IU/5×l06 cells. Examination of lymphocytes from patients with CLL revealed a marked decrease in UK activity as compared to normals (< 0.01 IU/5×106 cells in more than 50 % cases).The function of PA in normal lymphocyte physiology and the potential pathogenic role of diminished PA in CLL lymphocytes remains to be investigated.
7
Milivojević, Nevena, David Caballero, Mariana Carvalho, Marko Živanović, Nenad Filipovic, Rui Reis, and Joaquim Oliveira. "ENGINEERING A MICROFLUDIC PLATFORM AS A PRE-CLINICAL MODEL FOR BIOMEDICAL APPLICATIONS." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac,, 2021. http://dx.doi.org/10.46793/iccbi21.259m.
Full textAbstract:
Further technological advances are in great need for improving our understanding about critical biological and fundamental pathological processes, such as tissue development and cancer progression, or for the discovery and screening of novel pharmacological drugs. Preclinical experimentation demands for highly reliable and physiologically-relevant systems capable of recapitulating the complex human physiology. Traditional in vitro models, albeit widely employed, fail to reproduce the complexity of the native scenario with cells displaying aberrant gene expressions. Similarly, in vivo animal models, such as mice, poorly mimic the human condition and are ethically questionable. During the last decades, a new paradigm in preclinical modelling has emerged aiming to solve the limitations of the aforementioned methods. The combination of advanced tissue engineering, nanotechnology, and cell biology has resulted in the development of cutting-edge microfluidics-based models with an unprecedented ability to recreate within a microfluidic device the native habitat of cells within a microengineered chip. A diverse variety of micro- and bio-fabrication techniques is available for the development of microfluidic devices. Among all them, UV-photolithography and soft lithography is the considered the gold-standard method for the fabrication of chips due to its simplicity, versatility, and rapid prototyping. In this work, we describe the step-by-step fabrication procedure of a microfluidic chip by UV-photolithography and replica molding and discuss about their potential applications in the biomedical field.
8
Sharma, Puja, Kevin Sheets, and Amrinder S. Nain. "The Influence of Polymeric Fiber Stiffness and Alignment on Cytoplasmic Bleb Dynamics and Migration of Glioblastoma Multiforme Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80923.
Full textAbstract:
Cell migration is a tightly regulated phenomenon necessary for regular physiologic processes such as wound healing, immune response, embryonic development, growth, and regeneration [1–3]. Consequences of abnormal migratory behaviors include autoimmune diseases and metastasis during cancer progression [4, 5]. Described as one of the hallmarks of cancer, metastasis is a complex multistep process, and is responsible for 90% of cancer deaths in humans. A better understanding of the process of metastasis is of paramount importance in developing efficient cancer treatment therapies and drugs [6].
9
Richmond, Bonnie L., Kyle Damen, Ryan Moore, Alex White, and Julia H. Carter. "Abstract 3115: Physiologic comparisons of five bladder cancer cell lines." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3115.
Full text
10
Pryse, Kenneth M., Teresa M. Abney, Guy M. Genin, and Elliot L. Elson. "Probing Cytoskeletal Mechanics Using Biochemical Inhibitors." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19451.
Full textAbstract:
Quantifying the mechanics of the cytoskeletons of living cells is important for understanding several physiologic and pathologic cellular functions, such as wound healing and cellular migration in cancer. Our laboratory develops three-dimensional tissue constructs for assaying cytoskeletal mechanics in controlled conditions. These tissue constructs consist of defined components such as chick embryo fibroblasts and reconstituted rat tail collagen; fibroblasts remodel the collagen extracellular matrix (ECM) and develop a structural environment representative of that which would exist in a natural tissue. Our protocol for quantifying the microscale mechanics of the proteins that comprise the cytoskeleton involves mechanical testing of a tissue construct first in a bath that contains nutrition medium to support the active physiologic functioning of the cells, and next in the presence of inhibitors that selectively eliminate specific cytoskeletal structures. By solving an inverse homogenization problem, the mechanical functioning of these proteins at the cellular level can be estimated. Here, we present a combination of mechanical testing and imaging results to quantify the effects of specific inhibitors on cytoskeletal and extracellular matrix form and function.