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

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

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

Abstract 300: Regulation of androgen receptor transactivity and mTOR-S6 kinase pathway by Rheb in prostate cancer cell proliferation

2010 ◽  
Author(s):  
Takashi Kobayashi ◽  
Takahiro Inoue ◽  
Yosuke Shimizu ◽  
Naoki Terada ◽  
Toshinari Yamasaki ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cancer Cell Proliferation ◽  
S6 Kinase ◽  
Kinase Pathway

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 Tangeretin prevents prostate cancer cell proliferation and induces apoptosis via activation of Notch signalling and regulating the androgen receptor (AR) pathway and the phosphoinositide 3-kinase (PI3k)/Akt/mTOR pathways

2015 ◽  
Vol 10 (4) ◽  
pp. 937 ◽  
Author(s):  
Jin-Jin Guo ◽  
Ying-Jie Li ◽  
Lu-Lu Xin
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Specific Antigen ◽  
Significant Inhibition ◽  
Notch Signalling ◽  
Cancer Cell Proliferation ◽  
Apoptotic Proteins

<p class="Abstract">Despite advances in conventional therapies, treatment of prostate cancer is still a challenge. The study aims to assess the possible anti-cancer effects of tangeretin, a dietary flavonoid on human prostate cancer cells (DU145, PC3, LNCaP). Tangeretin (25, 50 and 100 µM) significantly inhibited cancer cell viability and induced DNA fragmentation and apoptosis by increasing caspase-3 and pro-apoptotic proteins (Bad and Bax) with reduced anti-apoptotic proteins (Bcl-2 and Bcl-xL) expressions. Significant inhibition of androgen receptor (AR) and prostate specific antigen (PSA) were seen. Dose-dependent inhibition in Notch signal was observed in expression of Notch 1 and Jagged 1 along with PI3/Akt/mTOR signalling pathway. The results suggest that tangeretin inhibited prostate cancer cell proliferation and induced apoptosis via inhibiting critical pathways in cancer development - AR signalling and PI3/Akt/mTOR - Notch signalling pathways.</p><p> </p>

scholarly journals 23-O-Substituted-2,3-Dehydrosilybins Selectively Suppress Androgen Receptor-Positive LNCaP Prostate Cancer Cell Proliferation

2020 ◽  
Vol 15 (5) ◽  
pp. 1934578X2092232
Author(s):  
Ziran Jiang ◽  
Arman Sekhon ◽  
Yogeshwari Oka ◽  
Guanglin Chen ◽  
Nagat Alrubati ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cell Proliferation ◽  
Androgen Receptor ◽  
Natural Product ◽  
Cancer Cell ◽  
Prostate Cancer Cell ◽  
Cell Model ◽  
Cancer Cell Proliferation ◽  
Castration Resistant Prostate Cancer ◽  
Lncap Prostate Cancer Cell

As part of our ongoing project to search for natural product-based antiandrogens, nine derivatives of 2,3-dehydrosilybin have been synthesized for the evaluation of its antiproliferative activity in an androgen receptor-positive prostate cancer cell model. Specifically, 3,5,7,20- O-tetramethyl-2,3-dehydrosilybin was synthesized through two approaches, and eight 23- O-substituted-3,5,7,20- O-tetramethyl-2,3-dehydrosilybins were achieved from 3,5,7,20- O-tetramethyl-2,3-dehydrosilybin. The antiproliferative potency of 3,5,7,20- O-tetramethyl-2,3-dehydrosilybin and its eight derivatives were assessed in an androgen receptor (AR)-positive LNCaP prostate cancer cell line, as well as in two AR-negative (PC-3 and DU145) prostate cancer cell models as a comparison. Our WST cell proliferation assay data indicate 3,5,7,20- O-tetramethyl-2,3-dehydrosilybin and most of its 23- O-substituents can selectively inhibit AR-positive LNCaP prostate cancer cell proliferation. Our data suggest that 3,5,7,20- O-tetramethyl-2,3-dehydrosilibins could serve as a natural product-based scaffold for new antiandrogens for lethal castration-resistant prostate cancer.

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