通过干细胞样重编程逃避靶向癌症治疗
Evasion of targeted cancer therapy through stem-cell-like reprogramming.
作者信息
Wadosky Kristine M, Ellis Leigh, Goodrich David W
机构信息
Department of Pharmacology & Therapeutics, Roswell Park Cancer Institute , Buffalo, NY, USA.
Department of Oncologic Pathology, Harvard Medical School, Brigham and Women's Hospital, Dana-Farber Cancer Institute , Boston, MA, USA.
出版信息
Mol Cell Oncol. 2017 Feb 16;4(2):e1291397. doi: 10.1080/23723556.2017.1291397. eCollection 2017.
Abstract
Prostate cancer variants expressing alternative lineage markers appear at relapse from antiandrogen therapy. We show that loss of the retinoblastoma () and tumor protein 53 () genes drives expression of stem cell reprogramming factors, lineage plasticity, and antiandrogen resistance. Epigenetic manipulation restores antiandrogen sensitivity-suggesting an approach for treating lethal prostate cancers.
摘要
表达替代性谱系标志物的前列腺癌变体在抗雄激素治疗复发时出现。我们发现，视网膜母细胞瘤（RB）和肿瘤蛋白53（p53）基因的缺失驱动了干细胞重编程因子的表达、谱系可塑性和抗雄激素抗性。表观遗传操作可恢复抗雄激素敏感性——这提示了一种治疗致命性前列腺癌的方法。
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本文引用的文献
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