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首页> 外文期刊>Molecular medicine reports >CSN5 silencing reverses sorafenib resistance of human hepatocellular carcinoma HepG2 cells
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CSN5 silencing reverses sorafenib resistance of human hepatocellular carcinoma HepG2 cells

机译:CSN5沉默可逆转人类肝癌HepG2细胞的索拉非尼耐药

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摘要

Hepatocellular carcinoma (HCC) is one of the most common tumor types, and is the third leading cause of cancer mortalities worldwide. A large number of patients with HCC are diagnosed at a late stage when the curative treatment of surgical resection and liver transplantation are no longer applicable. Sorafenib has been proved to improve overall survival in advanced HCC; however, drug resistance is common. The present study reported that the CSN5 is correlated with sorafenib resistance of the HCC cell line HepG2/S. Following silencing of CSN5, resistance to sorafenib was reversed, and multi-drug-resistance proteins, including as adenosine triphosphate binding cassette (ABC) B1, ABCC2 and ABCG2 as well as CDK6, cyclin D1 and B-cell lymphoma 2 were downregulated. In addition, it was demonstrated that the integrin beta-1, transforming growth factor-beta 1 and nuclear factor-kappa B pathways were modified by CSN5.
机译:肝细胞癌(HCC)是最常见的肿瘤类型之一,并且是全世界癌症死亡的第三大主要原因。当外科切除和肝移植的治愈性治疗不再适用时,大量晚期肝癌患者被诊断出来。索拉非尼已被证明可以改善晚期肝癌的整体生存率。但是,耐药性很普遍。本研究报道,CSN5与HCC细胞HepG2 / S的索拉非尼耐药性相关。 CSN5沉默后,对索拉非尼的耐药性被逆转,多重耐药蛋白包括三磷酸腺苷结合盒(ABC)B1,ABCC2和ABCG2以及CDK6,细胞周期蛋白D1和B细胞淋巴瘤2被下调。另外,证明了整联蛋白β-1,转化生长因子β1和核因子κB途径被CSN5修饰。

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