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USP9X 通过调控β-catenin 促进肝细胞癌的进展。

USP9X promotes the progression of hepatocellular carcinoma by regulating beta-catenin.

机构信息

Department of General Surgery, Weifang Yidu Central Hospital, Weifang, 262500, Shandong, China.

Department of Neurology, Weifang Yidu Central Hospital, Weifang, 262500, Shandong, China.

出版信息

Ir J Med Sci. 2020 Aug;189(3):865-871. doi: 10.1007/s11845-020-02199-2. Epub 2020 Feb 17.

DOI:10.1007/s11845-020-02199-2
PMID:32065347
Abstract

Hepatocellular carcinoma (HCC) is among the malignant tumors with highest mortality. The role of USP9X in the carcinogenesis of HCC has not yet been determined. In this study, USP9X was found significantly highly expressed in the intratumor tissues. Expression of intratumor USP9X was associated with tumor size and microvascular invasion while USP9X is independent risk factor of HCC disease-free survival and overall survival. In vitro studies revealed that knockdown of USP9X significantly inhibited the proliferation of HCC cells. Mechanically, USP9X promotes HCC cell proliferation by regulating the expression of beta-catenin. The results of the present study demonstrated that high expression of USP9X in intratumoral cells is associated with poor HCC prognosis, which may serve as a potential target for an adjuvant therapy.

摘要

肝细胞癌(HCC)是死亡率最高的恶性肿瘤之一。USP9X 在 HCC 发生中的作用尚未确定。在本研究中,发现 USP9X 在肿瘤内组织中显著高表达。肿瘤内 USP9X 的表达与肿瘤大小和微血管侵犯有关,而 USP9X 是 HCC 无病生存率和总生存率的独立危险因素。体外研究表明,USP9X 的敲低显著抑制 HCC 细胞的增殖。在机制上,USP9X 通过调节β-连环蛋白的表达促进 HCC 细胞增殖。本研究结果表明,肿瘤内细胞中 USP9X 的高表达与 HCC 预后不良相关,可能成为辅助治疗的潜在靶点。

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