scholarly journals Autophagy regulates lipolysis and cell survival through lipid droplet degradation in androgen-sensitive prostate cancer cells

The Prostate ◽  
2012 ◽  
Vol 72 (13) ◽  
pp. 1412-1422 ◽  
Author(s):  
Ramesh R. Kaini ◽  
Laurel O. Sillerud ◽  
Siqin Zhaorigetu ◽  
Chien-An A. Hu
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Lipid Droplet ◽  
Prostate Cancer Cells

scholarly journals Radiation-induced HIF-1α cell survival pathway is inhibited by soy isoflavones in prostate cancer cells

2009 ◽  
Vol 124 (7) ◽  
pp. 1675-1684 ◽  
Author(s):  
Vinita Singh-Gupta ◽  
Hao Zhang ◽  
Sanjeev Banerjee ◽  
Dejuan Kong ◽  
Julian J. Raffoul ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Soy Isoflavones ◽  
Prostate Cancer Cells ◽  
Survival Pathway ◽  
Radiation Induced

scholarly journals Cisplatin and Paclitaxel Modulated the Cell Survival Potential of Prostate Cancer Cells

Proceedings ◽  
2020 ◽  
Vol 40 (1) ◽  
pp. 42
Author(s):  
Kashani ◽  
Kilbas ◽  
Yerlikaya ◽  
Gurkan ◽  
Arisan
Keyword(s):  
Prostate Cancer ◽  
Cell Viability ◽  
Cell Survival ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Dependent Manner ◽  
Prostate Cancer Cells ◽  
Cell Viability Assay ◽  
Chemotherapy Drugs

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.

scholarly journals Androgen-induced lncRNA POTEF-AS1 regulates apoptosis-related pathway to facilitate cell survival in prostate cancer cells

2017 ◽  
Vol 108 (3) ◽  
pp. 373-379 ◽  
Author(s):  
Aya Misawa ◽  
Ken-ichi Takayama ◽  
Tetsuya Fujimura ◽  
Yukio Homma ◽  
Yutaka Suzuki ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Prostate Cancer Cells ◽  
Related Pathway

scholarly journals MicroRNA‑16‑5p regulates cell survival, cell cycle and apoptosis by targeting AKT3 in prostate cancer cells

2020 ◽  
Vol 44 (3) ◽  
pp. 1282-1292
Author(s):  
Fang Wang ◽  
Wendi Wang ◽  
Lina Lu ◽  
Yi Xie ◽  
Junfang Yan ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Survival ◽  
Cancer Cells ◽  
Prostate Cancer Cells

scholarly journals Targeting the USP1 dependent KDM4A protein stability as a potential prostate cancer therapy

2019 ◽  
Author(s):  
Shu-Zhong Cui ◽  
Ling-Ling Fan ◽  
You-Qiang Li ◽  
Xin-Yan Geng ◽  
De-Xue Fu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Survival ◽  
Cancer Cells ◽  
Real Time Pcr ◽  
Therapeutic Target ◽  
Knockout Mouse ◽  
Prostate Cancer Cell ◽  
Prostate Cancer Cells ◽  
Anti Cancer

Abstract Background: Prostate cancer is the most commonly diagnosed malignancy and second leading cause of cancer death in American men. The histone demethylase KDM4A is reported to be overexpressed and plays a vital in multiple cancers through controlling gene expression by epigenetic regulation of H3K9 or H3K36 methylation marks. The biological role and mechanism of KDM4A in regulating AR activity in prostate cancer, however, remain to be established. Methods: KDM4A expression in PTEN knockout mouse was determined using western blotting, Real-time PCR and immunohistochemical. Functional assays, such as cell survival, cell colony formation, anchorage-independent growth and a xenograft tumor model were used to determine the oncogenic role of KDM4A in prostate cancer cells. Association of KDM4A with USP1 and the deubiquitination assay were determined by co-immunoprecipitation, immunofluorescent staining and immunoblotting. USP1-KDM4A axis promotes AR-dependent c-Myc expression was further investigated using western blotting, chromatin immunoprecipitation and Real-time PCR. The specific USP1 inhibitor ML323 was used for assessing the role of USP1 in prostate cancer cell survival. Co-expression of KDM4A with USP1 was determined by immunohistochemical staining in 146 prostate cancer tissue samples. Results: Herein, we reported KDM4A expression was upregulation in PTEN knockout mouse prostate tissue. Depletion of KDM4A in prostate cancer cells inhibited their proliferation and survival in vivo and vitro. Further studies reveal that USP1 is a deubiquitinase that regulates KDM4A K48-linked deubiquitin and stability. Interestingly, we found c-Myc was a key downstream effector of USP1-KDM4A/AR axis in driving prostate cancer cell proliferation. Notably, upregulation of KDM4A expression with high USP1 expression were observed in 70% of prostate tumors and inhibition of USP1 promotes prostate cancer cells response to therapeutic agent_enzalutamide. Our studies propose USP1 may be an anti-cancer therapeutic target in prostate cancer. Conclusions: Our findings demonstrate that USP1 deubiquitinates and stabilizes KDM4A, which promotes recruitment of AR to the c-Myc gene enhancer and highlight USP1 potential as an anti-cancer therapeutic target in prostate cancer. Keywords: USP1; Prostate cancer; KDM4A; Deubiquitination; Tumorigenesis

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