下调和上调
前列腺癌
癌症研究
胆固醇
调节器
基因敲除
化学
流浪汉
前列腺
肿瘤进展
癌症
恶性肿瘤
转录组
药理学
脂质代谢
辛伐他汀
生物
癌细胞
体外
免疫印迹
转染
细胞培养
高胆固醇
肝X受体
医学
作者
Ye Zhi,Luqi Ge,Shaoru Wang,Wencong Zang,Zhentao Zhang,Tong Xu,Yiwen Zhang,Feifeng Song,Ping Huang
标识
DOI:10.1096/fj.202501885r
摘要
Prostate cancer (PCa) is a common and aggressive malignancy in men, often diagnosed at advanced stages with a poor five-year survival rate. Despite therapeutic advances, effective treatments for castration-resistant PCa remain lacking. Timosaponin A3 (TA3), a natural steroidal saponin derived from Anemarrhena asphodeloides Bunge, has shown potential anti-tumor properties, but its role in PCa and the underlying mechanisms have not been fully elucidated. In this study, we demonstrate that TA3 significantly inhibits the proliferation, migration, and invasion of PCa cells in vitro, and suppresses tumor growth in xenograft models. Transcriptomic analysis revealed that TA3 exerts its anti-tumor effects by modulating cholesterol metabolism. Elevated cholesterol levels were observed in PCa patients, and exogenous cholesterol administration reduced tumor growth in vivo. Notably, TA3 treatment upregulated the lipid transporter StAR related lipid transfer domain containing 4 (STARD4), a key regulator of cholesterol transport, which was confirmed to mediate the inhibitory effects of TA3 on PCa progression. Overexpression of STARD4 attenuated PCa development both in vitro and in vivo, while STARD4 knockdown abolished these effects. Collectively, our findings suggest that TA3 suppresses PCa progression by enhancing cholesterol metabolism via STARD4 upregulation, supporting its potential as a novel therapeutic agent for prostate cancer.
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