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首页> 外文期刊>Journal of cellular physiology. >Glycochenodeoxycholate induces cell survival and chemoresistance via phosphorylation of STAT3 at Ser727 site in HCC
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Glycochenodeoxycholate induces cell survival and chemoresistance via phosphorylation of STAT3 at Ser727 site in HCC

机译：Glycochenodeoxycholate诱发细胞生存和通过磷酸化STAT3在药物抗性HCC的Ser727

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摘要

Glycochenodeoxycholate (GCDA) is closely associated with carcinogenesis and chemoresistance of hepatocellular carcinoma (HCC). Signal transducer and activator of transcription 3 (STAT3), a transcription factor, is involved in various human tumors. Whether GCDA induces chemoresistance through STAT3 and the mechanism of action remains elusive. In this study, we firstly found that the expression level of STAT3 has a positive correlation with chemoresistance of HCC cells. Moreover, GCDA can upregulate the expression of STAT3 protein. Hence, we suspect that GCDA may induce chemoresistance of HCC cells via STAT3. Mechanistically, GCDA stimulates phosphorylation of STAT3 at Ser727 site and mediates pSer727-STAT3 protein to translocate and aggregate in the nucleus, which is important for cell survival. When Ser727 of STAT3 mutated to Asp, the capacity of STAT3 to accumulate in the nucleus was attenuated, STAT3-induced cell survival was impaired and GCDA-induced chemoresistance was abolished. In addition, while activation of extracellular signal-regulated kinase 1/2 (ERK1/2) was inhibited by PD98059, phosphorylation of STAT3 at Ser727 induced by GCDA was suppressed. Taken together, these data demonstrate that GCDA-enhanced survival of liver cancer cells may occur through the activation of STAT3 by phosphorylation at Ser727 site via mitogen-activated protein kinase/ERK1/2 pathway, which may contribute to the progression of human liver cancer and chemoresistance.
机译：Glycochenodeoxycholate (GCDA)密切与致癌作用和肝细胞癌的药物抗性(HCC)。转录因子转录3 (STAT3),参与多种人类肿瘤。通过STAT3和诱发药物抗性的作用机制仍然是难以捉摸的。研究中,我们首先发现表达水平STAT3的正相关肝癌细胞的药物抗性。移植STAT3蛋白的表达。因此,我们怀疑GCDA可能诱发通过STAT3肝癌细胞的药物抗性。从力学上看,GCDA刺激磷酸化STAT3在Ser727站点和协调pSer727-STAT3蛋白质可能促使和总在细胞核中,这是很重要的细胞的生存。Asp, STAT3积累的能力核是减毒,STAT3-induced细胞生存和GCDA-induced受损药物抗性被废除。激活细胞外signal-regulated由PD98059激酶1/2 (ERK1/2)被抑制,的磷酸化STAT3在Ser727诱导GCDA被抑制。证明GCDA-enhanced肝脏的生存通过激活肿瘤细胞可能发生通过磷酸化STAT3的Ser727网站增殖蛋白激酶/ ERK1/2通路,这可能导致人类的发展肝癌和药物抗性。

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