TRIM36, a novel androgen-responsive gene, enhances anti-androgen efficacy against prostate cancer by inhibiting MAPK/ERK signaling pathways.
TRIM36, a novel androgen-responsive gene, enhances anti-androgen efficacy against prostate cancer by inhibiting MAPK/ERK signaling pathways.
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TRIM36是一种新型雄激素反应基因，通过抑制MAPK/ERK信号通路增强抗前列腺癌的抗雄激素功效
DOI：
10.1038/s41419-017-0197-y
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发表时间：
2018-02-05
影响因子：
9
通讯作者：
Wang Z
中科院分区：
文献类型：
--
作者：
Liang C;Wang S;Qin C;Bao M;Cheng G;Liu B;Shao P;Lv Q;Song N;Hua L;Gu M;Li J;Wang Z
针对前列腺癌的激素治疗药物（如比卡鲁胺和恩杂鲁胺）主要关注雄激素受体（AR）信号传导，最初有效，但随着对这些药物耐药性的发展，疾病进展至致死性。延长药物反应时间和提高药物疗效的方法仍然不可用。TRIM 36被报道为一种新的雄激素信号传导靶基因，并且在前列腺癌中上调。在本研究中，我们发现63.4%（64/95）的TMA PCa表达TRIM 36蛋白。有趣的是，TRIM 36表达阴性的患者的生化无复发生存期较短。TRIM 36表达与Gleason评分显著相关（P= 0.005），延迟前列腺癌细胞周期进展，并在体外和体内抑制细胞增殖，这些作用通过抑制MAPK/ERK磷酸化途径介导。值得注意的是，我们发现在抗雄激素治疗期间拯救TRIM 36的表达可以提高药物疗效。总的来说，TRIM 36是一种新的雄激素反应基因，它显著增强了抗雄激素药物对前列腺癌的疗效。
Hormone therapy drugs, such as bicalutamide and enzalutamide, directed against prostate cancer focus on androgen receptor (AR) signaling and are initially effective, but the disease progresses to lethality as resistance to these drugs develops. A method to prolong the drug response time and improve the drug efficacy is still unavailable. TRIM36 was reported as a novel androgen signaling target gene and is upregulated in prostate cancer. In this study, we found that 63.4% (64/95) of PCa in TMA expressed the TRIM36 protein. Interestingly, patients with negative TRIM36 expression had a shorter biochemical recurrence-free survival. TRIM36 expression was significantly associated with the Gleason score (P= 0.005), delayed prostate cancer cell cycle progression and inhibited cell proliferation in vitro and in vivo, and these effects were mediated via inhibition of the MAPK/ERK phosphorylation pathway. Remarkably, we found that rescuing the expression of TRIM36 during anti-androgen therapy could improve the drug efficacy. Collectively, TRIM36 is a novel androgen-responsive gene, and it dramatically enhanced the efficacy of anti-androgen drugs against prostate cancer.
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影响因子：
64.5
作者：
Cawley, S;Bekiranov, S;Gingeras, TR
通讯作者：
Gingeras, TR
影响因子：
28.2
作者：
Nelson WG;Yegnasubramanian S
通讯作者：
Yegnasubramanian S
PKC epsilon 通过抑制肾细胞癌细胞系 769P 中的 ABCB1 转运蛋白和 PI3K/Akt、MAPK/ERK 信号传导来抑制侧群细胞的分离和严格性
影响因子：
9.7
作者：
Huang, Bin;Fu, Shun Jun;Qiu, Shao Peng
通讯作者：
Qiu, Shao Peng
DOI：
10.1056/nejmoa1315815
发表时间：
2014-09-11
期刊：
The New England journal of medicine
影响因子：
--
作者：
Antonarakis ES;Lu C;Wang H;Luber B;Nakazawa M;Roeser JC;Chen Y;Mohammad TA;Chen Y;Fedor HL;Lotan TL;Zheng Q;De Marzo AM;Isaacs JT;Isaacs WB;Nadal R;Paller CJ;Denmeade SR;Carducci MA;Eisenberger MA;Luo J
通讯作者：
Luo J
影响因子：
2.8
作者：
Song, Xuedong;Wang, Yin;Luo, Chunli
通讯作者：
Luo, Chunli