ACTR/AIB1/SRC-3 and androgen receptor control prostate cancer cell proliferation and tumor growth through direct control of cell cycle genes

The Prostate ◽  
2006 ◽  
Vol 66 (14) ◽  
pp. 1474-1486 ◽  
Author(s):  
June X. Zou ◽  
Zhenyu Zhong ◽  
Xu-Bao Shi ◽  
Clifford G. Tepper ◽  
Ralph W. deVere White ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Direct Control ◽  
Cell Cycle Genes

scholarly journals Osteoblasts Promote Prostate Cancer Cell Proliferation Through Androgen Receptor Independent Mechanisms

2021 ◽  
Vol 11 ◽  
Author(s):  
Giulia Ribelli ◽  
Sonia Simonetti ◽  
Michele Iuliani ◽  
Elisabetta Rossi ◽  
Bruno Vincenzi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Castration Resistant Prostate Cancer ◽  
Matrix Metalloproteinase 1 ◽  
Depth Analysis

Patients with metastatic prostate cancer frequently develop bone metastases that elicit significant skeletal morbidity and increased mortality. The high tropism of prostate cancer cells for bone and their tendency to induce the osteoblastic-like phenotype are a result of a complex interplay between tumor cells and osteoblasts. Although the role of osteoblasts in supporting prostate cancer cell proliferation has been reported by previous studies, their precise contribution in tumor growth remains to be fully elucidated. Here, we tried to dissect the molecular signaling underlining the interactions between castration-resistant prostate cancer (CRPC) cells and osteoblasts using in vitro co-culture models. Transcriptomic analysis showed that osteoblast-conditioned media (OCM) induced the overexpression of genes related to cell cycle in the CRPC cell line C4-2B but, surprisingly, reduced androgen receptor (AR) transcript levels. In-depth analysis of AR expression in C4-2B cells after OCM treatment showed an AR reduction at the mRNA (p = 0.0047), protein (p = 0.0247), and functional level (p = 0.0029) and, concomitantly, an increase of C4-2B cells in S-G2-M cell cycle phases (p = 0.0185). An extensive proteomic analysis revealed in OCM the presence of some molecules that reduced AR activation, and among these, Matrix metalloproteinase-1 (MMP-1) was the only one able to block AR function (0.1 ng/ml p = 0.006; 1 ng/ml p = 0.002; 10 ng/ml p = 0.0001) and, at the same time, enhance CRPC proliferation (1 ng/ml p = 0.009; 10 ng/ml p = 0.033). Although the increase of C4-2B cell growth induced by MMP-1 did not reach the proliferation levels observed after OCM treatment, the addition of Vorapaxar, an MMP-1 receptor inhibitor (Protease-activated receptor-1, PAR-1), significantly reduced C4-2B cell cycle (0.1 μM p = 0.014; 1 μM p = 0.0087). Overall, our results provide a novel AR-independent mechanism of CRPC proliferation and suggest that MMP-1/PAR-1 could be one of the potential pathways involved in this process.

scholarly journals Polar biophenolics in sweet potato greens extract synergize to inhibit prostate cancer cell proliferation and in vivo tumor growth

2013 ◽  
Vol 34 (9) ◽  
pp. 2039-2049 ◽  
Author(s):  
Sushma R. Gundala ◽  
Chunhua Yang ◽  
N. Lakshminarayana ◽  
Ghazia Asif ◽  
Meenakshi V. Gupta ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Sweet Potato ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation

scholarly journals Selective Androgen Receptor Modulator S42 Suppresses Prostate Cancer Cell Proliferation

Endocrinology ◽  
2018 ◽  
Vol 159 (4) ◽  
pp. 1774-1792 ◽  
Author(s):  
Takako Kawanami ◽  
Tomoko Tanaka ◽  
Yuriko Hamaguchi ◽  
Takashi Nomiyama ◽  
Hajime Nawata ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Selective Androgen Receptor Modulator ◽  
Receptor Modulator

Tip60 promotes prostate cancer cell proliferation by translocation of androgen receptor into the nucleus

The Prostate ◽  
2009 ◽  
Vol 70 (5) ◽  
pp. 540-554 ◽  
Author(s):  
Masaki Shiota ◽  
Akira Yokomizo ◽  
Daisuke Masubuchi ◽  
Yasuhiro Tada ◽  
Junichi Inokuchi ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation

LncRNA GAS5 participates in the regulation of dexamethasone on androgen receptor -negative and -positive prostate cancer cell proliferation

2020 ◽  
Vol 53 ◽  
pp. 101607
Author(s):  
Jieping Hu ◽  
Jun Deng ◽  
Runfu Cao ◽  
Shida Xiong ◽  
Ju Guo
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Lncrna Gas5

ADAM17 regulates prostate cancer cell proliferation through mediating cell cycle progression by EGFR/PI3K/AKT pathway

2011 ◽  
Vol 359 (1-2) ◽  
pp. 235-243 ◽  
Author(s):  
Ping Lin ◽  
Xicai Sun ◽  
Tian Feng ◽  
Haifeng Zou ◽  
Ying Jiang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Prostate Cancer Cell ◽  
Akt Pathway ◽  
Cancer Cell Proliferation ◽  
Cycle Progression

scholarly journals Knockdown of prostaglandin reductase 1 (PTGR1) suppresses prostate cancer cell proliferation by inducing cell cycle arrest and apoptosis

2016 ◽  
Vol 10 (2) ◽  
pp. 133-139 ◽  
Author(s):  
Li Xue ◽  
Zhen Zhu ◽  
Ziming Wang ◽  
Hecheng Li ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Arrest ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
Cycle Arrest
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