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转移性去势抵抗性前列腺癌的分子驱动因素:新的耐药途径。

Molecular drivers of metastatic castrate-resistant prostate cancer: New roads to resistance.

机构信息

a Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Bethesda , MD , USA.

出版信息

Cancer Biol Ther. 2018;19(10):869-870. doi: 10.1080/15384047.2018.1449618. Epub 2018 May 14.

Abstract

Numerous growth-inducing signaling pathways have been implicated in the development of metastatic castrate-resistant prostate cancer, but their cross-talk with androgen receptor functions remains poorly understood. A recent study published in Science Signaling by Chen et al. has identified a novel androgen-mediated signaling axis driven by loss of SPDEF and gain of TGFBI to facilitate metastasis, which may explain the acquisition of resistance to androgen deprivation therapy. These findings suggest that therapeutic inhibition of androgen signaling may inadvertently promote castrate resistance by inhibiting tumor suppressive functions of the androgen receptor.

摘要

许多促进生长的信号通路被认为与转移性去势抵抗性前列腺癌的发生有关,但它们与雄激素受体功能的相互作用仍知之甚少。最近,Chen 等人在《科学信号》杂志上发表的一项研究确定了一条新的雄激素介导的信号轴,该信号轴由 SPDEF 的缺失和 TGFBI 的获得驱动,从而促进转移,这可能解释了对雄激素剥夺治疗的耐药性的获得。这些发现表明,雄激素信号的治疗性抑制可能通过抑制雄激素受体的肿瘤抑制功能而无意中促进去势抵抗。

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本文引用的文献

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The transcription factor SPDEF suppresses prostate tumor metastasis.转录因子 SPDEF 抑制前列腺肿瘤转移。
J Biol Chem. 2012 Aug 24;287(35):29968-78. doi: 10.1074/jbc.M112.379396. Epub 2012 Jul 2.

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