Androgen suppresses PML protein expression in prostate cancer CWR22R cells.
Androgen suppresses PML protein expression in prostate cancer CWR22R cells.
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雄激素抑制前列腺癌 CWR22R 细胞中 PML 蛋白的表达。
DOI：
10.1016/j.bbrc.2003.12.060
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发表时间：
2004
影响因子：
3.1
通讯作者：
Chang,Chawnshang
中科院分区：
文献类型：
--
作者：
Yang,Lin;Yeh,Shauh-Der;Xie,Shaozhen;Altuwaijri,Saleh;Ni,Jing;Hu,Yueh-Chiang;Chen,Yen-Ta;Bao,Bo-Ying;Su,Ching-Hua;Chang,Chawnshang
PML能够调节肿瘤细胞中的关键抑制通路，提示PML可能是一种肿瘤抑制因子。然而，PML如何在前列腺癌进展中发挥作用的详细机制仍不清楚。在这里，我们证明了在雄激素存在的情况下，PML蛋白在CWR22R前列腺癌细胞中的表达可以被抑制。进一步的研究表明，PML可以选择性地抑制CWR22R细胞中AR的反式激活，并且PML蛋白的表达与p21蛋白水平的升高和P53转录能力的增强呈正相关。我们还发现PML强烈抑制CWR22R细胞集落形成，而PML siRNA增强AR活性和CWR22R细胞集落形成。总之，我们的结果表明，PML可能通过抑制AR反式激活和/或增强P53活性来抑制前列腺癌细胞的生长。
The ability of PML to modulate key suppressive pathways in tumor cells suggests that PML may act as a tumor suppressor. The detailed mechanism of how PML functions in prostate cancer progression, however, remains unknown. Here we demonstrate that in the presence of androgen, PML protein expression can be suppressed in CWR22R prostate cancer cells. Further studies reveal that PML can selectively suppress AR transactivation and PML protein expression positively correlates with increased p21 protein level and enhances p53 transcription ability in CWR22R cells. We also found that PML strongly inhibits CWR22R cell colony formation, while PML siRNA enhances AR activity and CWR22R cell colony formation. Together our results suggest that PML may suppress prostate cancer cell growth by inhibiting AR transactivation and/or enhancing p53 activity.