Relevant bibliographies by topics / Cell survival of prostate cancer cells

Academic literature on the topic 'Cell survival of prostate cancer cells'

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Published: 11 March 2023

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Journal articles on the topic "Cell survival of prostate cancer cells"

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Tindall, Donald J. "S1 Molecular Mechanisms of Prostate Cancer Cell Survival following Androgen Ablative Therapy." Japanese Journal of Urology 97, no. 2 (2006): 127. http://dx.doi.org/10.5980/jpnjurol.97.127_2.

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Cross, N. A., M. Papageorgiou, and C. L. Eaton. "Bone marrow stromal cells promote growth and survival of prostate cancer cells." Biochemical Society Transactions 35, no. 4 (July 20, 2007): 698–700. http://dx.doi.org/10.1042/bst0350698.

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Prostate cancers frequently metastasize to the skeleton, and it has been hypothesized that this environment selectively supports the growth of these tumours. Specifically there is strong evidence that interactions between tumour cells and BMSCs (bone marrow stromal cells) play a major role in supporting prostate cancer growth and survival in bone. Here, we examine factors shown to be secreted by BMSCs, such as IGFs (insulin-like growth factors) and IL-6 (interleukin 6), shown to promote prostate cancer cell proliferation and to potentially replace the requirement for androgens. In addition we discuss another factor produced by BMSCs, osteoprotegerin, which may promote tumour cell survival by suppressing the biological activity of the pro-apoptotic ligand TRAIL (tumour-necrosis-factor-related apoptosis-inducing ligand).
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Kashani, Kilbas, Yerlikaya, Gurkan, and Arisan. "Cisplatin and Paclitaxel Modulated the Cell Survival Potential of Prostate Cancer Cells." Proceedings 40, no. 1 (January 5, 2020): 42. http://dx.doi.org/10.3390/proceedings2019040042.

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Prostate cancer is the second common cause of death among men worldwide. In the treatment of prostate cancer, conventional chemotherapeutics are commonly used. The plant alkaloid Paclitaxel and platinum-based cisplatin are the most common chemotherapy drugs. The transcription factor p53 has a potential target in the regulation of cell response to DNA damage of prostate cancer. Although the effectiveness of these drugs on prostate cancer cell progression had been proved, the mechanistic action of these drugs on the progression of the disease is not detailed explained. In this study, we aim to examine the function of p53 overexpression in prostate cancer cell survival. Therefore, we treated wild type (wt) and p53 overexpressed PC3 (p53+) prostate cancer cells with cisplatin or paclitaxel. According to the MTT Cell Viability assay, cisplatin (12.5–25–50 µM) was found to be more effective decreasing PC3 and PC3 p53+ cell viability in a dose-dependent manner compared to paclitaxel (12.5–25–50 nM). Colony formation assay showed that treatment of cells with cisplatin or paclitaxel caused the loss of colony forming ability of PC3 and PC3 p53+ cells. In addition, the critical apoptotic markers Caspase-3 and Caspase-9 expressions were altered with cisplatin or paclitaxel treated PC3 wt and p53+ cells.
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LEE, E. C. Y., and M. TENNISWOOD. "PROGRAMMED CELL DEATH AND SURVIVAL PATHWAYS IN PROSTATE CANCER CELLS." Archives of Andrology 50, no. 1 (January 2004): 27–32. http://dx.doi.org/10.1080/01485010490250498.

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Salih, T., K. Aziz, S. Thiyagarajan, M. Armour, B. Shanmugam, J. Zeng, S. J. Adam, D. W. Felsher, T. L. DeWeese, and P. T. Tran. "Radiosensitization of MYC-overexpressing prostate cancer cells by statins." Journal of Clinical Oncology 29, no. 7_suppl (March 1, 2011): 26. http://dx.doi.org/10.1200/jco.2011.29.7_suppl.26.

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26 Background: Studies have shown a link between HMG-CoA reductase inhibitors (statins) and decreased cancer risk in various cancers including prostate cancer. Recent clinical studies have shown improved outcome for men on statin therapy receiving definitive radiation therapy compared to radiation therapy alone for prostate cancer. The oncogene Ras can be inhibited by statin treatment and in turn also result in targeted downregulation of Myc. Inactivation of Myc has been shown to induce tumor regression in transgenic mouse models of different cancers. Methods: Utilizing both in vitro and in vivo models, we studied in MYC over-expressing prostate cancer cells statin induced cytotoxicity and radiosensitization. We studied the effect of statin treatment with and without radiation treatment on in vitro cell death and clonogenic survival and correlated effects to levels of MYC and phospho-MYC. We constructed mutant cell lines to specifically examine the MYC-dependent effects of statins on prostate cancer cell cytotoxicity and radiosensitization. We performed similar studies in vivo using subcutaneous tumor grafts. Results: Statin treatment alone of prostate cancer cells resulted in increased cell death and decreased clonegenic survival. Statin treatment further sensitized prostate cancer cells to ionizing radiation as shown through colony formation assays. These cellular effects were associated with decreased levels of active MYC as confirmed by western and phospho-western analysis. Statin-induced cell death and decreased MYC levels could be rescued with the HMG-CoA bypass product mevalonate. Finally, flank tumor graft experiments demonstrated the ability of statins and radiation to delay tumor growth in vivo. Conclusions: Our preliminary data have implicated MYC as a potential critical target for the cytotoxic effects of statins on prostate cancer cells. The prevalence of MYC overexpression in human prostate cancers is as high as 80%. Thus the ability of statins to radiosensitize MYC overexpressing prostate cancer cells may provide a mechanistic explanation to the improved outcomes for men taking statins while on radiation therapy and now may afford us a molecular biomarker to examine this phenomenon in the clinic. No significant financial relationships to disclose.
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Mamouni, Kenza, Georgios Kallifatidis, and Bal L. Lokeshwar. "Targeting Mitochondrial Metabolism in Prostate Cancer with Triterpenoids." International Journal of Molecular Sciences 22, no. 5 (February 28, 2021): 2466. http://dx.doi.org/10.3390/ijms22052466.

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Metabolic reprogramming is a hallmark of malignancy. It implements profound metabolic changes to sustain cancer cell survival and proliferation. Although the Warburg effect is a common feature of metabolic reprogramming, recent studies have revealed that tumor cells also depend on mitochondrial metabolism. Due to the essential role of mitochondria in metabolism and cell survival, targeting mitochondria in cancer cells is an attractive therapeutic strategy. However, the metabolic flexibility of cancer cells may enable the upregulation of compensatory pathways, such as glycolysis, to support cancer cell survival when mitochondrial metabolism is inhibited. Thus, compounds capable of targeting both mitochondrial metabolism and glycolysis may help overcome such resistance mechanisms. Normal prostate epithelial cells have a distinct metabolism as they use glucose to sustain physiological citrate secretion. During the transformation process, prostate cancer cells consume citrate to mainly power oxidative phosphorylation and fuel lipogenesis. A growing number of studies have assessed the impact of triterpenoids on prostate cancer metabolism, underlining their ability to hit different metabolic targets. In this review, we critically assess the metabolic transformations occurring in prostate cancer cells. We will then address the opportunities and challenges in using triterpenoids as modulators of prostate cancer cell metabolism.
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Dariane, Charles, Sylvie Clairefond, Benjamin Péant, Laudine Communal, Zhe Thian, Véronique Ouellet, Dominique Trudel, et al. "High Keratin-7 Expression in Benign Peri-Tumoral Prostatic Glands Is Predictive of Bone Metastasis Onset and Prostate Cancer-Specific Mortality." Cancers 14, no. 7 (March 23, 2022): 1623. http://dx.doi.org/10.3390/cancers14071623.

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Background: New predictive biomarkers are needed to accurately predict metastasis-free survival (MFS) and cancer-specific survival (CSS) in localized prostate cancer (PC). Keratin-7 (KRT7) overexpression has been associated with poor prognosis in several cancers and is described as a novel prostate progenitor marker in the mouse prostate. Methods: KRT7 expression was evaluated in prostatic cell lines and in human tissue by immunohistochemistry (IHC, on advanced PC, n = 91) and immunofluorescence (IF, on localized PC, n = 285). The KRT7 mean fluorescence intensity (MFI) was quantified in different compartments by digital analysis and correlated to clinical endpoints in the localized PC cohort. Results: KRT7 is expressed in prostatic cell lines and found in the basal and supra-basal compartment from healthy prostatic glands and benign peri-tumoral glands from localized PC. The KRT7 staining is lost in luminal cells from localized tumors and found as an aberrant sporadic staining (2.2%) in advanced PC. In the localized PC cohort, high KRT7 MFI above the 80th percentile in the basal compartment was significantly and independently correlated with MFS and CSS, and with hypertrophic basal cell phenotype. Conclusion: High KRT7 expression in benign glands is an independent biomarker of MFS and CSS, and its expression is lost in tumoral cells. These results require further validation on larger cohorts.
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Jähnisch, Hanka, Susanne Füssel, Andrea Kiessling, Rebekka Wehner, Stefan Zastrow, Michael Bachmann, Ernst Peter Rieber, Manfred P. Wirth, and Marc Schmitz. "Dendritic Cell-Based Immunotherapy for Prostate Cancer." Clinical and Developmental Immunology 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/517493.

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Dendritic cells (DCs) are professional antigen-presenting cells (APCs), which display an extraordinary capacity to induce, sustain, and regulate T-cell responses providing the opportunity of DC-based cancer vaccination strategies. Thus, clinical trials enrolling prostate cancer patients were conducted, which were based on the administration of DCs loaded with tumor-associated antigens. These clinical trials revealed that DC-based immunotherapeutic strategies represent safe and feasible concepts for the induction of immunological and clinical responses in prostate cancer patients. In this context, the administration of the vaccine sipuleucel-T consisting of autologous peripheral blood mononuclear cells including APCs, which were pre-exposedin vitroto the fusion protein PA2024, resulted in a prolonged overall survival among patients with metastatic castration-resistent prostate cancer. In April 2010, sipuleucel-T was approved by the United States Food and Drug Administration for prostate cancer therapy.
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Harris, Koran S., and Bethany A. Kerr. "Prostate Cancer Stem Cell Markers Drive Progression, Therapeutic Resistance, and Bone Metastasis." Stem Cells International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/8629234.

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Metastatic or recurrent tumors are the primary cause of cancer-related death. For prostate cancer, patients diagnosed with local disease have a 99% 5-year survival rate; however, this 5-year survival rate drops to 28% in patients with metastatic disease. This dramatic decline in survival has driven interest in discovering new markers able to identify tumors likely to recur and in developing new methods to prevent metastases from occurring. Biomarker discovery for aggressive tumor cells includes attempts to identify cancer stem cells (CSCs). CSCs are defined as tumor cells capable of self-renewal and regenerating the entire tumor heterogeneity. Thus, it is hypothesized that CSCs may drive primary tumor aggressiveness, metastatic colonization, and therapeutic relapse. The ability to identify these cells in the primary tumor or circulation would provide prognostic information capable of driving prostate cancer treatment decisions. Further, the ability to target these CSCs could prevent tumor metastasis and relapse after therapy allowing for prostate cancer to finally be cured. Here, we will review potential CSC markers and highlight evidence that describes how cells expressing each marker may drive prostate cancer progression, metastatic colonization and growth, tumor recurrence, and resistance to treatment.
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Pulukuri, Sai MuraliKrishna, Christopher S. Gondi, Sajani S. Lakka, Aman Jutla, Norman Estes, Meena Gujrati, and Jasti S. Rao. "RNA Interference-directed Knockdown of Urokinase Plasminogen Activator and Urokinase Plasminogen Activator Receptor Inhibits Prostate Cancer Cell Invasion, Survival, and Tumorigenicity in Vivo." Journal of Biological Chemistry 280, no. 43 (August 26, 2005): 36529–40. http://dx.doi.org/10.1074/jbc.m503111200.

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The invasive ability of tumor cells plays a key role in prostate cancer metastasis and is a major cause of treatment failure. Urokinase plasminogen activator-(uPA) and its receptor (uPAR)-mediated signaling have been implicated in tumor cell invasion, survival, and metastasis in a variety of cancers. This study was undertaken to investigate the biological roles of uPA and uPAR in prostate cancer cell invasion and survival, and the potential of uPA and uPAR as targets for prostate cancer therapy. uPA and uPAR expression correlates with the metastatic potential of prostate cancer cells. Thus, therapies designed to inhibit uPA and uPAR expression would be beneficial. LNCaP, DU145, and PC3 are prostate cancer cell lines with low, moderate, and high metastatic potential, respectively, as demonstrated by their capacity to invade the extracellular matrix. In this study we utilized small hairpin RNAs (shRNAs), also referred to as small interfering RNAs, to target human uPA and uPAR. These small interfering RNA constructs significantly inhibited uPA and uPAR expression at both the mRNA and protein levels in the highly metastatic prostate cancer cell line PC3. Our data demonstrated that uPA-uPAR knockdown in PC3 cells resulted in a dramatic reduction of tumor cell invasion as indicated by a Matrigel invasion assay. Furthermore, simultaneous silencing of the genes for uPA and uPAR using a single plasmid construct expressing shRNAs for both uPA and uPAR significantly reduced cell viability and ultimately resulted in the induction of apoptotic cell death. RNA interference for uPA and uPAR also abrogated uPA-uPAR signaling to downstream target molecules such as ERK1/2 and Stat 3. In addition, our results demonstrated that intratumoral injection with the plasmid construct expressing shRNAs for uPA and uPAR almost completely inhibited established tumor growth and survival in an orthotopic mouse prostate cancer model. These findings uncovered evidence of a complex signaling network operating downstream of uPA-uPAR that actively advances tumor cell invasion, proliferation, and survival of prostate cancer cells. Thus, RNA interference-directed targeting of uPA and uPAR is a convenient and novel tool for studying the biological role of the uPA-uPAR system and raises the potential of its application for prostate cancer therapy.
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Dissertations / Theses on the topic "Cell survival of prostate cancer cells"

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Wilce, Alice J. "Understanding the function and mechanisms of intestinal cell kinase in the growth and survival of prostate cancer cells." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/85439/1/Alice_Wilce_Thesis.pdf.

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This project was a step forward in discovering the potential role of intestinal cell kinase in prostate cancer development. Intestinal cell kinase was shown to be upregulated in prostate cancer cells and altered expression led to changes in key cell survival proteins. This study used in vitro experiments to monitor changes in cell growth, protein and RNA expression.
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Zhang, Xiaomeng. "Significance and molecular basis of Id-1 in regulation of cancer cell survival and invasion." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39325477.

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Faysal, Joanne M. "The Effects of Hypoxia with Concomitant Acidosis on Prostate Cancer Cell Survival." Scholarly Repository, 2010. http://scholarlyrepository.miami.edu/oa_theses/69.

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Prostate cancer is the second most common cancer among men in the United States. While treatments for prostate cancer exist, none are curative. As a solid tumor, prostate cancer can grow beyond the diffusion limits of oxygen, thereby resulting in a hypoxic environment. While hypoxia can cause death to a variety of cell types, tumor cells can develop resistance to hypoxia and survive under minimal oxygen conditions. Hypoxia in tumor cells has also been associated with poor prognosis, increased metastasis, and decreased efficacy of chemotherapy. BNIP3, a BH-3 only proapoptotic Bcl-2 family member, has been shown to play an important role in cell death under hypoxic conditions in a variety of cell types. In normoxia, BNIP3 shows little to no expression in both cardiomyocytes and many cancer cell types, but is then upregulated under hypoxic conditions. Previous work in our laboratory provides evidence that hypoxia alone, as well as the concomitant increase in BNIP3 expression, cannot cause death of rat neonatal cardiomyocytes. Instead, our studies found that hypoxia with concomitant intracellular acidosis is required. Further studies indicated that BNIP3 is also necessary for hypoxia-acidosis associated cell death in cardiomyocytes. Our results in rat neonatal cardiomyocytes led us to hypothesize that cell death could be induced in hypoxic prostate cancer cells if concomitant acidosis could be induced. Additionally, our intention was to determine if BNIP3 was required for any prostate cancer cell death that may occur under hypoxia-acidosis conditions.
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Win, Hla Yee. "Role of protein kinase C-iota in prostate cancer." [Tampa, Fla.] : University of South Florida, 2008. http://purl.fcla.edu/usf/dc/et/SFE0002322.

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Zhang, Xiaomeng, and 張效萌. "Significance and molecular basis of Id-1 in regulation of cancer cell survival and invasion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39325477.

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Soori, Mehrnoosh. "Neuroendocrine differentiation of prostate cancer cells a survival mechanism during early stages of metastatic colonization of bone /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 105 p, 2009. http://proquest.umi.com/pqdweb?did=1654490661&sid=6&Fmt=2&clientId=8331&RQT=309&VName=PQD.

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Ekman, Maria. "The role of Smad7 and TRAF6 in Prostate Cancer Cell Invasion, Migration and Survival." Doctoral thesis, Uppsala universitet, Ludwiginstitutet för cancerforskning, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-159150.

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Transforming growth factor (TGF) β is a tumor suppressor during early tumor development, by inhibiting proliferation and inducing apoptosis. At later stages of cancer, it becomes a tumor promoter, and promotes tumor cell migration and invasion. TGFβ signals via its type II and type I receptors to several downstream signaling pathways. In the present work we have focused on the TRAF6 (tumor necrosis factor receptor-associated factor 6)/ TAK1 (TGFβ activated kinase 1) signaling pathway and the Smad7-dependent activation of p38 in prostate carcinoma cells (PC3U). We found that TGFβ-induced activation of the ubiquitin ligase TRAF6 was needed for cell invasion, by a mechanism that involves activation of the metalloproteinase TNFα converting enzyme (TACE), via protein kinase Cζ (PKCζ). TACE cleaves the TβRI, whereafter the intracellular domain (ICD) translocates to the nucleus, where it binds to the transcriptional co-activator p300 and regulates gene expression, promoting invasion. Interestingly, the translocation of the TβRI ICD was observed in several cancer cell lines and in sections of primary tumors, but not in primary prostate epithelial cells. We also found that Smad7 and adenomatous polyposis coli (APC) are important for TGFβ- and epidermal growth factor (EGF)-induced cell migration in PC3U cells. TGFβ induces the formation of a complex consisting of Smad7, p38, glycogene synthase kinase 3β (GSK-3β), APC and β-catenin, which localizes to the membrane ruffles in the leading edge of migrating cells. The complex links the TβRI to the microtubule system and promotes membrane ruffling and microtubule polarization, which are known to be important for cell migration. In the EGF signaling pathway, Smad7 was found to be important for phosphorylation of the EGF receptor at Tyr1068, for the activation of p38 and JNK, and for induction of membrane ruffles. Smad7 is required for TGFβ-induced activation of p38 and apoptosis. We found that Smad7 forms a complex with p38 and ataxia telangiectasia mutated (ATM), which is important for activation of p53 mediated apoptosis. Many tumor cells including the PC3U cells lack a functional p53, which is one of the reasons to why cancer cells can avoid the tumor suppressor effects of TGFβ.
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Armstrong, Chris. "Inhibition of treatment-induced cell survival signalling enhances radiosensitivity of PTEN-deficient prostate cancer." Thesis, Queen's University Belfast, 2015. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.680869.

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Loss of the tumour suppressor PTEN is a common feature of prostate cancer (PCa) and has recently been identified as a prognostic factor for patient relapse following radiotherapy. Published studies in our laboratory have identified CXCL8 signalling as a mediator of PTEN-depleted disease progression and therapeutic resistance. Therefore, experiments were designed to determine whether ionising radiation (IR) could selectively induce CXCL8 signalling in PTEN-deficient cells. Furthermore, we aimed to determine whether therapeutic targeting of the CXCL8 pathway could enhance PCa cell radiosensitivity. The results in this thesis show how exposure to IR increased gene and protein expression of CXCL8. In addition, inhibiting CXCL8 signalling with receptor-targeted siRNA or peptides increased PTEN-depleted cell sensitivity to IR. In vivo, treatment of PTEN-deficient xenografts with IR and a CXCR1/2-targeted pepducin (x1/2pal-i3) resulted in significant tumour growth delay. Subsequent analysis of tumour material confirmed that this was mediated by modulation of IR-induced anti-apoptotic proteins. Similar to CXCL8 signalling, macrophage infiltration has been associated with enhanced disease progression and poor therapeutic outcomes in prostate cancer patients. Unpublished data in our . laboratory has shown that loss of PTEN can predict for macrophage infiltration in prostate patient samples. Experiments were therefore designed to determine the impact of IR on macrophage-mediated paracrine signalling. Using the THP-1 cell line to model the macrophage component, co-culture systems demonstrated that the presence of microenvironment cells can enhance prostate cancer cell radioresistance. Furthermore, IR was shown to induce secretion of the cytokine TNF-α and this was sufficient to initiate NFKB-mediated upregulation of anti-apoptotic protein expression. Inhibition of cellular inhibitor of apoptosis protein-1 (clAP-1) by Smac-mimetics overcame TNF-α pro-survival effects and reduced cell viability by 50%. In addition, pre-treatment with Smac-mimetics sensitised DU145 cells to ionising radiation following macrophage co-culture.
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BUSA', ROBERTA. "Role of the RNA-binding protein Sam68 in prostate cancer cell survival and proliferation." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2009. http://hdl.handle.net/2108/908.

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Il tumore prostatico si sviluppa come una iper-proliferazione dipendente dagli androgeni delle cellule epiteliali ghiandolari e viene inizialmente affrontato con una terapia anti-androgenica. Tuttavia, dopo una regressione iniziale, il tumore si evolve in una forma più aggressiva indipendente dagli androgeni per cui ad oggi non è stata ancora trovata una cura (Grossmann et al., 2001). Nel nostro laboratorio è stata precedentemente descritta l’attivazione della tirosin chinasi Src in un gruppo di tumori prostatici avanzati, correlata alla fosforilazione in tirosina della RNA-binding protein Sam68 (Pronetto et al., 2004) appartenente alla famiglia STAR (Signal transduction and RNA metabolism), coinvolta nello splicing e nel processamento dei pre-mRNA (Lukong and Richard, 2003). Da qui abbiamo analizzato l’espressione e la funzione di Sam68 in cellule tumorali. Abbiamo osservato che, nei pazienti affetti da PCa, Sam68 è up-regolata sia a livello di mRNA che a livello di proteina. La down-regolazione di Sam68 tramite RNAi o interferire con la sua funzione in vivo con una proteina chimerica (GFP-Sam68GSG ) determinano un rallentamento della proliferazione di cellule tumorali prostatiche e le rendono più suscettibili all’apoptosi indotta da agenti chemoterapici. Questi dati mostrano quindi che l’espressione di Sam68 favorisce la proliferazione delle cellule tumorali di prostata e la sopravvivenza ad agenti chemoterapici (Busà et al., 2007). Ci siamo poi concentrati sullo studio del ruolo di Sam68 in questi eventi a livello molecolare. Abbiamo osservato che nelle cellule PC3, una linea di tumore prostatico non responsiva agli androgeni, in seguito a trattamento con l’agente chemoterapico mitoxantrone Sam68 rilocalizza all’interno di granuli nucleari. Abbiamo caratterizzato questi granuli nucleari ed abbiamo visto che in essi Sam68 colocalizza con diverse RNA-binding protein, sia appartenenti alla famiglia SR (SC35 e ASF/SF2) sia coinvolte nella risposta cellulare allo stress(hnRNP A1 e TIA1) (Guil et al., 2006). Sam68 si accumula anche in granuli citoplasmatici in cui co-localizza sia con hnRNP A1 che con TIA1, confermando si tratti dei cosiddetti stress granules (SGs). Questi dati suggeriscono che Sam68 faccia parte di una risposta cellulare allo stress “RNA-mediata”. Inoltre, poiché questa proteina è in grado di legare gli mRNA e di mediare lo splicing alternativo di pre-mRNA, abbiamo cercato di identificare i target modulati dal trattamento con il chemoterapico. In particolare ci siamo concentrati sullo splicing alternativo di un target già noto di Sam68, CD44 (Matter et al., 2002). Siamo andati ad analizzare lo splicing alternativo del pre-mRNA di CD44 in seguito a una dose-risposta con il mitoxantrone ed abbiamo riscontrato delle variazioni di splicing di alcuni esoni variabili, in particolare per v5 e v6, che sono noti essere regolati da Sam68 (Matter et al., 2002; Cheng and Sharp, 2006). Per valutare se le differenze osservate sono dovute alla rilocalizzazione di Sam68 effettueremo trattamenti con il chemoterapico su cellule silenziate per Sam68. Abbiamo individuato le vie biochimiche e di trasduzione del segnale che si accendono in risposta al trattamento con il mitoxantrone, la via del DNA damage di ATM e la via delle MAPkinasi indotta da stress di JNK1/2 e p38. Attraverso l’uso di inibitori specifici, per ATM, p38 e JNK, abbiamo osservato che queste vie non sono necessarie per la rilocalizzazione di Sam68. E ‘ dunque possibile che cambiamenti di conformazione della cromatina stimolino l’accumulo si Sam68 ed altri splicing factors nei granuli nucleari. Infine, alcune evidenze emerse nel corso dei nostri studi suggeriscono un nuovo ruolo di Sam68 nel metabolismo degli rRNA. In un esperimento di co-immunoprecipitazione per Sam68, tra le proteine lin grado di interagire con Sam68 abbiamo identificato Nucleolina, una proteina nucleolare coinvolta nel metabolismo del rRNA (Rickards et al., 2007). Abbiamo confermato quest’interazione e mappato la regione di legame nel dominio carbossi-terminale di Sam68. Inoltre, in un esperimento di co-immunoprecipitazione per Sam68 ed RNA, abbiamo identificato il 18S rRNA tra gli RNA legati da questa proteina. Abbiamo inoltre osservato, attraverso esperimenti di FISH confermati poi da real time PCR, che la down-regolazione di Sam68 determina un aumento significativo dei livelli del pre-rRNA in confronto alle cellule di controllo. Infine esperimenti di ChIP hanno dimostrato che Sam68 è in grado di legare il rDNA a cavallo della regione codificante per il 18S rRNA. Questi risultati suggeriscono un nuovo ruolo di Sam68 nel metabolismo del pre-rRNA. References: Busà R, Paronetto MP, Farini D, Pierantozzi E, Botti F, Angelini DF, Attisani F, Vespasiani G, Sette C., Oncogene 2007 26(30):4372-82. Cheng C, Sharp PA. (2006). Regulation of CD44 alternative splicing by SRm160 and its potential role in tumor cell invasion. Mol Cell Biol. 26(1):362-70. Grossmann ME, Tindall DJ (2001). Androgen receptor signaling in androgen-refractory prostate cancer. J Natl Cancer Inst. 93:1687-97; Guil S, Long JC, Cáceres JF. (2006). hnRNP A1 relocalization to the stress granules reflects a role in the stress response. Mol Cell Biol. 26(15):5744-58. Lukong KE, Richard S (2003). Sam68, the KH domain-containing superSTAR. Bioch. Biophys. Acta 1653: 73-86. Matter N, Herrlich P, Konig H (2002). Signal-dependent regulation of splicing via phosphorylation of Sam68. Nature 420:691-695. Paronetto MP, Farini D, Sammarco I, Maturo G, Vespasiani G, Geremia R et al (2004). Expression of a truncated form of the c-Kit tyrosine kinase receptor and activation of Src kinase in human prostatic cancer. Am. J. Path. 164:1243-1251; Rickards B, Flint SJ, Cole MD, LeRoy G. (2007). Nucleolin is required for RNA polymerase I transcription in vivo. Mol Cell Biol. 27(3):937-48.
Prostate carcinoma (PCa) is one of the main causes of death in the western male population. Although initially controlled by anti-androgenic therapies, PCa often evolves to become androgen-insensitive and highly metastatic. A predominant role in the development of androgen-refractoriness is played by the upregulation of signal transduction pathways that allow prostate cancer cells to autonomously produce their own requirements of growth factors and nutrients (Grossmann et al., 2001). The tyrosine kinase Src is frequently activated in advanced human prostate carcinomas and in our laboratory we have observed that its activation correlates with tyrosine phosphorylation of the RNA-binding protein Sam68 (Paronetto et al., 2004), belonging to the STAR family (Signal transduction and RNA metabolism) and involved in RNA metabolism. In the first part of this PhD Thesis, we have investigated the expression and function of Sam68 in human prostate cancer cells. We observed that Sam68 is up-regulated both at protein and mRNA levels in patients affected by PCa. Moreover, it was observed that down-regulation of Sam68 by RNAi in LNCaP prostate cancer cells delayed cell cycle progression, reduced the proliferation rate and sensitized cells to apoptosis induced by DNA-damaging agents. Microarray analyses revealed that a subset of genes involved in proliferation and apoptosis were altered when Sam68 was knocked down in LNCaP cells. Finally, stable cell lines expressing a truncated GFP-Sam68GSG protein, that interacts with endogenous Sam68 affecting its activity, displayed reduced growth rates and higher sensitivity to cisplatin-induced apoptosis, resembling down-regulation of Sam68 by RNAi. Together, these results indicate that Sam68 expression supports prostate cancer cells proliferation and survival to cytotoxic agents (Busà et al., 2007). Stemming from this evidence, we then aimed to investigate the role played by Sam68 in the response to genotoxic drugs such as mitoxantrone (MTX), a topoisomerase II inhibitor.We observed that MTX caused a subcellular re-localization of Sam68 from nucleoplasm to nuclear granules. Co-staining experiments indicated that Sam68-positive nuclear granules are sites of accumulation of several RNA-binding proteins involved in alternative splicing, such as SR proteins like SC35 and ASF/SF2, and TIA-1 and hnRNP A1, involved in cellular stress responses to various stimuli (Guil et al., 2006). Sam68 also accumulated in cytoplasmic granules that were also co-stained with hnRNP A1 and TIA-1, suggesting that these structures are the well described cytoplasmic stress granules (SGs). These data strongly suggest that Sam68 is part of a RNA-mediated stress response of the cell. Thus, we have begun to investigate whether changes in subcellular localization of Sam68 induced by genotoxic drugs affect alternative splicing of Sam68 target mRNAs, such as CD44 (Matter et al., 2002). Preliminary experiments have shown that MTX treatment in PC3 cells induces changes in alternative splicing of CD44 pre-mRNA. In particular, inclusion of variable exons v5 and v6, known to be regulated by Sam68 (Matter et al., 2002; Cheng and Sharp, 2006), was stimulated. We are current extending these studies to determine whether downregulation of Sam68 by RNAi affects these modifications of CD44 alternative splicing caused by MTX Since Sam68 is known to link signal transduction pathways to RNA metabolism (Lukong and Richard, 2003), we asked whether changes in Sam68 subcellular localization induced by MTX are determined by activation of specific signal transduction pathways. Our data show that although MTX triggers activation of DNA damage pathway, through ATM kinase, and stress-induced MAPKs p38 and JNK1/2 pathways, specific inhibition of these pathways did not affect the subcellular relocalization of Sam68. Thus, it is possible that direct changes in the chromatin structure or function trigger the observed accumulation of Sam68 and splicing factors in nuclear granules. Finally, a set of observations performed during our studies implicate Sam68 in nucleolar functions. In a co-immunoprecipitation experiment aimed at the identification of Sam68-interacting proteins in LNCaP cells we found Nucleolin, a nucleolar protein involved in rRNA metabolism (Rickards et al., 2007). This interaction has been confirmed and mapped to the carboxyterminal region of Sam68 by in vitro studies. Moreover, a RNA-protein co-immunoprecipitation experiment revealed that Sam68 binds 18S rRNA These observations lead us to investigate whether Sam68 plays a role in rRNA metabolism. First, we observed by FISH analysis, and then confermed by real time PCR, that downregulation of Sam68 caused a significant increase in the levels of pre-rRNA compared with control siRNA treated cells. Moreover, ChIP assays aimed at determining the site of the association of Sam68 with rDNA in PC3 cells revealed that Sam68 binds the 18S rRNA coding region. Thus, the results presented herein strongly suggest a novel role of Sam68 in the regulation of pre-rRNA maturation. Our current studies are aimed at investigating this hypothesis further. References: Busà R, Paronetto MP, Farini D, Pierantozzi E, Botti F, Angelini DF, Attisani F, Vespasiani G, Sette C., Oncogene 2007 26(30):4372-82. Cheng C, Sharp PA. (2006). Regulation of CD44 alternative splicing by SRm160 and its potential role in tumor cell invasion. Mol Cell Biol. 26(1):362-70. Grossmann ME, Tindall DJ (2001). Androgen receptor signaling in androgen-refractory prostate cancer. J Natl Cancer Inst. 93:1687-97; Guil S, Long JC, Cáceres JF. (2006). hnRNP A1 relocalization to the stress granules reflects a role in the stress response. Mol Cell Biol. 26(15):5744-58. Lukong KE, Richard S (2003). Sam68, the KH domain-containing superSTAR. Bioch. Biophys. Acta 1653: 73-86. Matter N, Herrlich P, Konig H (2002). Signal-dependent regulation of splicing via phosphorylation of Sam68. Nature 420:691-695. Paronetto MP, Farini D, Sammarco I, Maturo G, Vespasiani G, Geremia R et al (2004). Expression of a truncated form of the c-Kit tyrosine kinase receptor and activation of Src kinase in human prostatic cancer. Am. J. Path. 164:1243-1251; Rickards B, Flint SJ, Cole MD, LeRoy G. (2007). Nucleolin is required for RNA polymerase I transcription in vivo. Mol Cell Biol. 27(3):937-48.
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Eng, Grace Tzi Ai. "An investigation of the effect of some stable nitroxide antioxidants in prostate cancer cells." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/82982/4/Grace_Eng_Thesis.pdf.

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The risk of prostate cancer and disease progression may potentially be increased by oxidative stress. This project examined the stability of nitroxide antioxidants and their effects on cell growth, survival and gene regulation in prostate cancer cells. The novel nitroxide, CTMIO, synthesised here at QUT, was found to have minimal toxicity and modulated the expression of a subset of oxidative stress and antioxidant-related genes distinct from those regulated by a related derivative. This study has provided a step forward in our understanding of the mechanism of action of nitroxides within cells.
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Books on the topic "Cell survival of prostate cancer cells"

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Meridith, Alan T. Handbook of prostate cancer cell research: Growth, signalling, and survival. New York: Nova Biomedical Books, 2009.

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T, Meridith Alan, ed. Handbook of prostate cancer cell research: Growth, signalling, and survival. Hauppauge, NY: Nova Science, 2009.

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Handbook of prostate cancer cell research: Growth, signalling, and survival. New York: Nova Biomedical Books, 2009.

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Sardinian International Meeting on Modulating Factors in Multistage Chemical Carcinogenesis (5th 1989 Cagliari, Italy). Chemical carcinogenesis 2: Modulating factors. New York: Plenum Press, 1991.

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Clarke, Noel W. Metastatic disease in prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0068.

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Metastases are the predominant cause of morbidity and death from prostate cancer (CaP). The tendency for cells to migrate from the primary site, enter the vascular/lymphatic circulation, and implant/grow at secondary sites is the principal discriminator of aggressive form indolent disease. But this process is poorly understood. Cells enter the circulation in increasing number as the disease progresses, impinging on endothelial surfaces, particularly in red bone marrow where they bind and transmigrate, forming early cell colonies. This requires chemo-attractants and nutrients enabling cellular survival. Established metastases thrive independently, disrupting local tissue, as characterized by progressive replacement of red bone marrow and disruption of skeletal architecture. Bone disruption includes massive overstimulation of both osteoblasts and osteoclasts, inducing synchronous over-production of abnormal bone and gross osteolysis.
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Meridith, Alan T. Handbook of Prostate Cancer Cell Research: Growth, Signalling and Surviva. Nova Science Publishers, Incorporated, 2009.

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Grant, Warren, and Martin Scott-Brown. Prevention of cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0350.

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In the UK, the four commonest cancers—lung cancer, breast cancer, colon cancer, and prostate cancer—result in around 62 000 deaths every year. Although deaths from cancer have fallen in the UK over the last 20 years, the UK still suffers from higher cancer death rates than many other countries in Western Europe. In 1999, the UK government produced a White Paper called Saving Lives: Our Healthier Nation that outlined a national target to reduce the death rate from cancer by at least 20% in people under 75 by 2010. The subsequent NHS Cancer Plan of 2000 designed a framework by which to achieve this target through effective prevention, screening, and treatment programmes as well as restructuring and developing new diagnostic and treatment facilities. But do we know enough about the biology of the development of cancer for government health policies alone to force dramatic changes in survival? The science behind the causes of cancer tells us that its origin lies in acquired or inherited genetic abnormalities. Inherited gene mutation syndromes and exposure to environmental mutagens cause cancer, largely through abnormalities in DNA repair mechanisms, leading to uncontrolled cell proliferation. Although screening those thought to be at highest risk, and regulating exposure to environmental carcinogens such as tobacco or ionizing radiation, have reduced, and will continue to reduce, cancer deaths, there are many other environmental factors that have been shown to increase the population risk of cancer. These will be outlined in this chapter. However, the available evidence is largely from retrospective and cross-sectional population-based studies and therefore limits the ability to apply this knowledge to the risk of the individual patient who may been seen in clinic. Although we may be able to put him or her into a high-, intermediate-, or low-risk category, the question ‘will I get cancer, doc?’ is one that we cannot answer with certainty. The NHS Cancer Plan of 2000, designed to reduce cancer deaths in this country and to bring UK treatment results in line with those other countries in Europe, focuses on preventing malignancy as part of its comprehensive cancer management strategy. It highlights that the rich are less likely to develop cancer, and will survive longer if they are diagnosed than those who live in poverty. This may reflect available treatment options, but is more likely to be related to the lifestyle of those with regular work, as they may be more health aware. The Cancer Plan, however, suggests that relieving poverty may be more labour intensive and less rewarding than encouraging positive risk-reducing behaviour in all members of the population. Eating well can reduce the risk of developing many cancers, particularly of the stomach and bowel. The Cancer Plan outlines the ‘Five-a-Day’ programme which was rolled out in 2002 and encouraged people to eat at least five portions of fruit and vegetables per day. Obese people are also at higher risk of cancers, in particular endometrial cancer. A good diet and regular exercise not only reduce obesity but are also independent risk-reducing factors. Alcohol misuse is thought to be a major risk factor in around 3% of all cancers, with the highest risk for cancers of the mouth and throat. As part of the Cancer Plan, the Department of Health promotes physical activity and general health programmes, as well as alcohol and smoking programmes, particularly in deprived areas. Focusing on these healthy lifestyle points can potentially reduce an individual lifetime risk of all cancers. However, our knowledge of the biology of four cancers in particular has led to the development of specific life-saving interventions. Outlined in this chapter are details regarding ongoing prevention strategies for carcinomas of the lung, the breast, the bowel, and the cervix.
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Eisen, Tim. The patient with renal cell cancer. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0172.

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Renal cancer is the commonest malignancy of the kidney and worldwide, accounts for between 2% and 3% of the total cancer burden. The mainstay of curative treatment remains surgery. There have been significant advances in surgical technique, the most important ones being nephron-sparing surgery and laparoscopic nephrectomy. The medical treatment of advanced renal cell cancer has only improved markedly in the last decade with the development of antiangiogenic tyrosine-kinase inhibitors, inhibitors of mammalian target of rapamycin, and a diminished role for immunotherapy.Tyrosine-kinase inhibitor therapy results in reduction of tumour volume in around three-quarters of patients and doubles progression-free survival, but treatment is not curative. The management of side effects in patients on maintenance tyrosine-kinase inhibitors has improved in the last 3 years, although still presents difficulties which have to be actively considered.The molecular biology of renal cell carcinoma is better understood than for the majority of solid tumours. The commonest form of renal cancer, clear-cell carcinoma of the kidney, is strongly associated with mutations in the von Hippel–Lindau gene and more recently with chromatin-remodelling genes such as PBRM1. These genetic abnormalities lead to a loss of control of angiogenesis and uncontrolled proliferation of tumour cells. There is a very wide spectrum of tumour behaviour from the extremely indolent to the terribly aggressive. It is not currently known what accounts for this disparity in tumour behaviour.A number of outstanding questions are being addressed in scientific and clinical studies such as a clearer understanding of prognostic and predictive molecular biomarkers, the role of adjuvant therapy, the role of surgery in the presence of metastatic disease, how best to use our existing agents, and investigation of novel targets and therapeutic agents, especially novel immunotherapies.
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Farghaly, Samir A. Adoptive Cell Immunotherapy for Epithelial Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0005.

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The standard management for epithelial ovarian cancer (EOC) is a combination of aggressive debulking surgery with residual tumor of less than 1 cm and platinum-based chemotherapy. However, a high percentage of patients experience disease recurrence. Extensive efforts to find new therapeutic options have been made, albeit cancer cells develop drug resistance and malignant progression occurs. Novel therapeutic strategies are needed to enhance progression-free survival and overall survival of patients with advanced EOC. Several preclinical and clinical studies investigated feasibility and efficacy of adoptive cell therapy (ACT) in EOC. The aim of this chapter is to present an overview of ACT in EOC, focusing on Human Leukocyte Antigen (HLA)-restricted tumor infiltrating lymphocytes and MHC-independent immune effectors such as natural killer and cytokine-induced killer. The available data suggest that ACT may provide the best outcome in patients with low tumor burden, minimal residual disease, or maintenance therapy. Further preclinical studies and clinical trials are needed.
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(Editor), A. Columbano, F. Feo (Editor), P. Pani (Editor), and R. Pascale (Editor), eds. Chemical Carcinogenesis, Volume 2: Modulating Factors. Plenum Press, 1991.

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Book chapters on the topic "Cell survival of prostate cancer cells"

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Buczek, Magdalena E., Jerome C. Edwards, and Tarik Regad. "Prostate Cancer and Prostate Cancer Stem Cells." In Principles of Stem Cell Biology and Cancer, 193–212. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118670613.ch10.

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Badeaux, Mark A., and Dean G. Tang. "Prostate Cancer Cell Heterogeneity and Prostate Cancer Stem Cells." In Cancer Stem Cells, 183–91. Hoboken, NJ: John Wiley & Sons, 2014. http://dx.doi.org/10.1002/9781118356203.ch14.

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Moscatelli, David, and E. Lynette Wilson. "The Prostate Stem Cell Niche." In Stem Cells and Prostate Cancer, 91–109. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6498-3_6.

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Liu, Qingxin, Yun Zhang, Danielle Jernigan, and Alessandro Fatatis. "Survival and Growth of Prostate Cancer Cells in the Bone: Role of the Alpha-Receptor for Platelet-Derived Growth Factor in Supporting Early Metastatic Foci." In Signaling Pathways and Molecular Mediators in Metastasis, 261–75. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2558-4_11.

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Chanda, Diptiman, and Selvarangan Ponnazhagan. "Mesenchymal Stem Cells in Prostate Cancer." In Stem Cell Therapeutics for Cancer, 171–85. Hoboken, NJ: John Wiley & Sons, Inc, 2013. http://dx.doi.org/10.1002/9781118660423.ch13.

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Joshi, Molishree U., Courtney K. von Bergen, and Scott D. Cramer. "Targeting the Prostate Stem Cell for Chemoprevention." In Stem Cells and Prostate Cancer, 127–48. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6498-3_8.

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Ulkus, Lindsey, Min Wu, and Scott D. Cramer. "Stem Cell Models for Functional Validation of Prostate Cancer Genes." In Stem Cells and Prostate Cancer, 149–73. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6498-3_9.

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Klein, Sandra, Fiona M. Frame, and Norman J. Maitland. "Therapy Resistance in Prostate Cancer: A Stem Cell Perspective." In Stem Cells: Current Challenges and New Directions, 279–300. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8066-2_13.

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Chang, Woochul, Byeong-Wook Song, and Ki-Chul Hwang. "Mesenchymal Stem Cell Survival in Infarcted Myocardium: Adhesion and Anti-death Signals." In Stem Cells and Cancer Stem Cells, Volume 10, 35–43. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6262-6_4.

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Ichikawa, T., Y. Furuya, K. Akakura, and J. Shimazaki. "Growth-Stimulating Effect of Growth Factor(s) from Androgen Independent Tumor Cells (CS 2-Cell) on Androgen Responsive Tumor Cells (SC 115-Cell)." In Molecular and Cellular Biology of Prostate Cancer, 279. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3704-5_29.

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Conference papers on the topic "Cell survival of prostate cancer cells"

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Su, Fengmin, Yiming Fan, He Xu, Nannan Zhao, Yangbo Deng, Yulong Ji, and Hongbin Ma. "Ultra-High Speed Vitrification of Prostate Cancer Cells Based on Thin Film Evaporation." In ASME 2019 6th International Conference on Micro/Nanoscale Heat and Mass Transfer. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/mnhmt2019-3910.

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Abstract Thin film evaporation is an efficient phase change heat transfer style, and could achieve ultra-high cooling rate if it was applied for cells vitrification. In this paper, an experimental study for prostate cancer cells vitrification was done. The cells ultra-high speed freezing method was based on thin film evaporation of liquid nitrogen. In order to examine the feasibility of the new method, the comparison experiments, in which the other two generic approaches of cell cryopreservation were used, were done. The methods were respectively the equilibrium freezing method and the open pulled straws vitrification method. At the same time, the influences of the concentration of cryoprotectant on cooling rate and cell survival rate were analyzed. The results showed that the ultra-high speed freezing method based on thin film evaporation can obtain higher cooling rate and better cell survival rate than the other two conventional cryopreservation methods. It preliminarily proved the feasibility of this method applied to the cells vitrification process. In addition, both the cooling rate and the cell survival rate are affected by the concentration of the cryoprotectant in the cell suspension. The cooling rate decreases with the concentration of the cryoprotectant increasing, but cell survival rate increases first and decrease afterwards with the increase of the concentration of the cryoprotectant, in which an optimum value exists. This study will promote the practicality of the new ultra-fast cell freezing method.
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Chetram, Mahandranauth A., Danaya A. Bethea, Taylor J. Stowers, and Cimona V. Hinton. "Abstract 538: ROS differentially regulates prostate cancer cell survival." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-538.

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Kreutz, Fernando T. "Abstract A029: Cell-based cancer immunotherapy using tumor presenting cells: A phase II trial with local advance prostate cancer patients." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a029.

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Chang, Megan, Micaela Morgado, Viral Patel, Michael Gwede, Mary Cindy Farach-Carson, and Nikki Delk. "Abstract B15: Bone marrow stromal cell-secreted inflammatory cytokines promote treatment resistance and survival of prostate cancer cells." In Abstracts: AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment; February 26 — March 1, 2014; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-b15.

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Niture, Suresh, Malathi Ramalinga, Habib Kedir, and Deepak Kumar. "Abstract 2342: TNFAIP8 promotes prostate cancer cell survival by modulating autophagy." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-2342.

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Baraket, David, Jing Zhang, Theresa Barberi, Alan D. Friedman, and Ido Paz-Priel. "Abstract 841: The role of C/EBPβ in prostate cancer cell survival." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-841.

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Too, Catherine K. L., Lynn N. Thomas, and Jennifer Merrimen. "Abstract 86: Prolactin and testosterone induction of carboxypeptidase-D to promote cell survival is greater in prostate cancer cells than benign prostate cells, and their synergistic action in prostate cancer cells is effectively blocked by receptor antagonists Δ1-9-G129R and flutamide." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-86.

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Tanaka, Mai, Samantha S. Dykes, and Dietmar W. Siemann. "Abstract 2507: Axl suppression inhibits cell migration, invasion and survival in breast and prostate 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.am2018-2507.

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Liang, Yayun, Benford Mafuvadze, Xiaoqin Zou, Cynthia Besch-Williford, and Salman M. Hyder. "Abstract 5422: Inhibition of oxidosqualene cyclase blocks proliferation and survival of prostate cancer cells." 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.am2015-5422.

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Goulart, Ana Emilia, Luciana B. Ferreira, Paula Priscilla de Freitas, Nadia Batoreu, MARTIN H. BONAMINO, and Etel Rodrigues Pereira Gimba. "Abstract 163: Investigation of molecular mechanisms by which PCA3 modulates prostate cancer cell survival." 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.am2015-163.

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Reports on the topic "Cell survival of prostate cancer cells"

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McCarthy, James B., and Eva Turley. Hyaluronan Tumor Cell Interactions in Prostate Cancer Growth and Survival. Fort Belvoir, VA: Defense Technical Information Center, December 2009. http://dx.doi.org/10.21236/ada525644.

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McCarthy, James B., and Eva Turley. Hyaluronan Tumor Cell Interactions in Prostate Cancer Growth and Survival. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada470057.

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Elledge, Stephen. Identification of Genes Required for the Survival of Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2011. http://dx.doi.org/10.21236/ada547231.

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Elledge, Stephen J. Identificaton of Genes Required for the Survival of Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, June 2010. http://dx.doi.org/10.21236/ada552841.

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Knudsen, Beatrice S. Control of Prostate Cancer Cell Growth and Survival by the Extracellular Matrix. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada371208.

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Huang, Wen-Chin. A Novel Anti-Beta2-Microglobulin Antibody Inhibition of Androgen Receptor Expression, Survival, and Progression in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2010. http://dx.doi.org/10.21236/ada545568.

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Huang, Wen-Chin. A Novel Anti-Beta2-Microglobulin Antibody Inhibition of Androgen Receptor Expression, Survival, and Progression in Prostate Cancer Cells. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada561161.

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Brooks, James D. Single Cell Characterization of Prostate Cancer-Circulating Tumor Cells. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada596639.

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Brooks, James B. Single Cell Characterization of Prostate Cancer Circulating Tumor Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2011. http://dx.doi.org/10.21236/ada550987.

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Pizzo, Salvatore, and Robin E. Bachelder. Targeting Prostate Cancer Stemlike Cells through Cell Surface-Expressed GRP78. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613546.

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