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首页> 外文期刊>Cancer Cell >FKBP51 affects cancer cell response to chemotherapy by negatively regulating Akt.
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FKBP51 affects cancer cell response to chemotherapy by negatively regulating Akt.

机译：FKBP51通过负调节Akt影响癌细胞对化疗的反应。

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摘要

Akt is a central regulator of cell growth. Its activity can be negatively regulated by the phosphatase PHLPP that specifically dephosphorylates the hydrophobic motif of Akt (Ser473 in Akt1). However, how PHLPP is targeted to Akt is not clear. Here we show that FKBP51 (FK506-binding protein 51) acts as a scaffolding protein for Akt and PHLPP and promotes dephosphorylation of Akt. Furthermore, FKBP51 is downregulated in pancreatic cancer tissue samples and several cancer cell lines. Decreased FKBP51 expression in cancer cells results in hyperphosphorylation of Akt and decreased cell death following genotoxic stress. Overall, our findings identify FKBP51 as a negative regulator of the Akt pathway, with potentially important implications for cancer etiology and response to chemotherapy.
机译：Akt是细胞生长的中央调节剂。磷酸酶PHLPP可以使Akt的疏水基序（Akt1中的Ser473）特异地磷酸化，从而对其活性进行负调节。但是，PHLPP如何针对Akt尚不清楚。在这里，我们显示FKBP51（FK506结合蛋白51）充当Akt和PHLPP的支架蛋白，并促进Akt的去磷酸化。此外，FKBP51在胰腺癌组织样品和几种癌细胞系中下调。癌细胞中FKBP51表达的减少导致Akt的过度磷酸化并降低了遗传毒性应激后的细胞死亡。总体而言，我们的发现将FKBP51鉴定为Akt途径的负调节剂，对癌症病因和对化疗的反应具有潜在的重要意义。

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