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首页> 外文期刊>Journal of cellular physiology. >LINC00205 modulates the expression of EPHX1 through the inhibition of miR-184 in hepatocellular carcinoma as a ceRNA
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LINC00205 modulates the expression of EPHX1 through the inhibition of miR-184 in hepatocellular carcinoma as a ceRNA

机译：LINC00205调节EPHX1的表达通过抑制mir - 184肝细胞癌作为龙头

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摘要

Several studies have shown that low expression of epoxide hydrolase 1 (EPHX1) is closely associated with varying human cancers, including hepatocellular carcinoma (HCC). This study aims to explore the potential mechanism of EPHX1 silencing and revealed a novel regulatory pathway in the pathogenesis of HCC. In this study, micro ribonucleic acid (miR)-184 was predicted and validated to be a regulator of EPHX1 through experiments, and its expression was negatively correlated with the messenger RNA (mRNA) levels of EPHX1 in primary tumors. Elevation of EPHX1 suppressed cell proliferation and migration as well as cell cycle progression, and induced apoptosis, while downregulation of miR-184 exhibited the opposite effect on cellular processes. Moreover, LINC00205 interacted with miR-184 and was markedly downregulated in tumors. The effects of the miR-184 inhibitor on cell proliferation, apoptosis, and migration were reversed in part by the transfection with LINC00205 small interfering RNAs. In addition, LINC00205 acted as a molecular sponge to positively regulate the mRNA and protein levels of EPHX1 via regulating miR-184. The tumorigenicity of HCC cells was enhanced by LINC00205 shRNA but diminished by overexpression of EPHX1 in vivo. Clinically, the EPHX1 expression in patients with HCC was markedly downregulated. Taken together, the results of this study suggest that as a competing endogenous RNA, LINC00205 may regulate EPHX1 by inhibiting miR-184 in the progression of HCC and that targeting the LINC00205/miR-184/ EPHX1 axis may provide a treatment protocol for patients.
机译：多项研究表明,低表达环氧化物水解酶1 (EPHX1)是密切相关的不同的人类癌症,包括肝细胞癌(HCC)。探索EPHX1的潜在机制沉默和揭示了一种新的监管途径在肝细胞癌的发病机制。核糖核酸(miR) -184年预测验证的调节器EPHX1通过实验,其表达式是消极的与信使核糖核酸(mRNA)水平EPHX1的主要肿瘤。抑制细胞增殖和迁移细胞周期进展,以及诱导的差别细胞凋亡,而对这些mir - 184细胞表现出相反的效果流程。mir - 184和在肿瘤明显下调。mir - 184抑制剂对细胞的影响增殖、凋亡和迁移部分逆转转染LINC00205小干扰rna。LINC00205分子海绵积极规范mRNA和蛋白水平通过调节EPHX1 mir - 184。肝癌细胞的致瘤性增强了LINC00205 shRNA但减少过度EPHX1体内。表达肝细胞癌患者是明显的表达下调。本研究表明,作为一个内生的竞争RNA, LINC00205可能调节EPHX1通过抑制mir - 184肝癌的进展针对LINC00205 mir - 184 / EPHX1轴为病人提供治疗协议。

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