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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >DIAPH3 promoted the growth, migration and metastasis of hepatocellular carcinoma cells by activating beta-catenin/TCF signaling
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DIAPH3 promoted the growth, migration and metastasis of hepatocellular carcinoma cells by activating beta-catenin/TCF signaling

机译:通过激活β-catenin / TCF信号传导,DiaPH3促进肝细胞癌细胞的生长,迁移和转移

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摘要

The enhanced ability of cancer cell migration and metastasis is the major cause for the cancer-related death of hepatocellular carcinoma (HCC). Better understanding the mechanisms for the motility of cancer cells will benefit the treatment. Diaphanous-related formin 3 (DIAPH3) has been reported to regulate the motility of cells by remodeling the cytoskeleton. However, the mechanism through which DIAPH3 regulated the motility of cancer cells remains largely unknown. In this study, we have shown that the expression of DIAPH3 was up-regulated in HCC. DIAPH3 positively regulated the growth, migration, colony formation, epithelia mesenchymal transition, and metastasis of HCC cells. Mechanically, DIAPH3 activated the beta-catenin/TCF signaling by binding HSP90 and disrupting the interaction between GSK3beta and HSP90. Taken together, our study demonstrated the oncogenic activity of DIAPH3 in the progression of HCC and suggested that PDIAPH3 might be a therapeutic target.
机译:癌细胞迁移和转移的增强能力是肝细胞癌(HCC)癌症相关死亡的主要原因。 更好地理解癌细胞运动的机制将有益于治疗。 据报道,透明相关的甲素3(DiaPH3)通过重塑细胞骨架来调节细胞的动力。 然而,Diaph3调节的机制受癌细胞的动力仍然未知。 在本研究中,我们已经表明,Diaph3的表达在HCC中占据了升级。 DIAPH3积极地调节生长,迁移,菌落形成,上皮细胞间充质转换和HCC细胞转移。 机械地,DIAPH3通过结合HSP90并破坏GSK3BETA和HSP90之间的相互作用来激活β-连环蛋白/ TCF信号传导。 我们的研究表明,在HCC进展中,表明DIAPH3的致癌活性,并表明PDIAPH3可能是治疗目标。

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