Undesirable Status of Prostate Cancer Cells after Intensive Inhibition of AR Signaling: Post-AR Era of CRPC Treatment.
Undesirable Status of Prostate Cancer Cells after Intensive Inhibition of AR Signaling: Post-AR Era of CRPC Treatment.
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强烈抑制AR信号传导后，前列腺癌细胞的不良状态：CRPC治疗后的AR ERA。
DOI：
10.3390/biomedicines9040414
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发表时间：
2021-04-12
期刊：
影响因子：
4.7
通讯作者：
Mizokami A
中科院分区：
文献类型：
--
作者：
Makino T;Izumi K;Mizokami A
前列腺癌（PC）研究的最新进展揭示了去势抵抗性PC（CRPC）中雄激素受体（AR）的真实的功能。此外，AR仍然通过激活几种机制（例如，CRPC中的突变、变体和扩增）。基于AR诱导CRPC进展的这些无可争议的机制，开发了新一代AR信号靶向药物，极大地抑制了AR的活性。然而，AR信号靶向药物的长期给药随后诱导的主要问题是AR（完全）非依赖性CRPC细胞既不呈现AR也不呈现前列腺特异性抗原，包括作为AR非依赖性CRPC亚型的神经内分泌分化。此外，很少有证据表明对AR非依赖性CRPC有效的治疗方法。本研究主要探讨AR依赖性CRPC细胞向AR非依赖性CRPC转化的机制以及AR非依赖性CRPC的潜在治疗策略，并结合基础和临床文献进行讨论。
Recent advances in prostate cancer (PC) research unveiled real androgen receptor (AR) functions in castration-resistant PC (CRPC). Moreover, AR still accelerates PC cell proliferation via the activation of several mechanisms (e.g., mutation, variants, and amplifications in CRPC). New-generation AR signaling-targeted agents, inhibiting extremely the activity of AR, were developed based on these incontrovertible mechanisms of AR-induced CRPC progression. However, long-term administration of AR signaling-targeted agents subsequently induces the major problem that AR (complete)-independent CRPC cells present neither AR nor prostate-specific antigen, including neuroendocrine differentiation as a subtype of AR-independent CRPC. Moreover, there are few treatments effective for AR-independent CRPC with solid evidence. This study focuses on the transformation mechanisms of AR-independent from AR-dependent CRPC cells and potential treatment strategy for AR-independent CRPC and discusses them based on a review of basic and clinical literature.
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影响因子：
21.3
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影响因子：
82.9
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