摘要
前列腺癌的发生、进展依赖于雄激素,因此去势手术成为治疗晚期前列腺癌的标准疗法。但是去势后大多前列腺癌最终将转化为雄激素非依赖性前列腺癌,甚至进展为激素难治性前列腺癌,使得肿瘤的进展不受低水平雄激素的影响。即使如此,大多数激素非依赖性前列腺癌,依然阳性表达雄激素受体。因而雄激素受体在前列腺癌发生发展中起着重要作用。而PI3K/Akt信号通路能够通过维持细胞生存、抑制细胞凋亡、促进细胞代谢及血管生成等促进前列腺癌进展。本综述旨在总结前人研究,阐述雄激素受体和PI3K/Akt信号通路之间相互作用关系。研究表明Akt信号通路能够正性或者负性调控AR蛋白表达、蛋白的稳定性及其转录活性,从而维持细胞的生存、代谢。而AR即可以通过基因转录途径抑制Akt活化又能通过非转录基因途径激活Akt及其下游蛋白。因此,AR和Akt信号通路相互协同促进前列腺癌的发生及其向雄激素非依赖性前列腺癌进展。
The growth of prostate cancer dependent on androgen,however most of prostate cancer may result in progression to androgen independence after ADT（androgen deprived therapy）.Even so androgen receptors express in majority of androgen indepen-dent prostate cancer.Therefore androgen receptor is important in the progression of prostate cancer.The Akt signaling pathway promotes the aggressive of prostate cancer,by the maintenance of cell survival,cell metabolism and angiogenesis,inhibiting apoptosis.In this review,we described interaction between androgen receptor and the Akt signaling pathways by summarizing previous research.Akt sig-naling pathway can be positive or negative regulation of AR protein expression,and its stability and transcriptional activity,thereby maintaining cell survival,metabolism.In addition,androgens regulate the Akt pathway by both genomic and non-genomic effects.The synergy between Akt and AR signaling that is sufficient to initiate and progress native adult murine prostatic epithelium to frank carcino-ma and override the effect of androgen ablation.
出处
《现代生物医学进展》
CAS
2011年第1期180-183,共4页
Progress in Modern Biomedicine
基金
国家自然科学基金(30600618)
关键词
雄激素受体
前列腺癌
AKT
Prostate cancer
Androgen receptor
PI3K
Akt
