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首页> 外文期刊>Cellular Physiology and Biochemistry >Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma
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Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

机译：长时间非编码MALAT1作为竞争性内源RNA来调节海绵状miR-30a-5p在肝细胞癌中调节波形蛋白的表达。

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Background/Aims Hepatocellular carcinoma (HCC) has a high morbidity as well as mortality and is believed to be one of the most prevalent cancers worldwide. The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in numerous cancers, including HCC. This study aimed to explore the role of MALAT1 in HCC progression. Methods The expression levels of MALAT1 and Vimentin in HCC tissues and relative pair-matched adjacent normal liver tissues were analyzed by RT-PCR, and immunohistochemistry. Using bioinformatics analysis and dual-luciferase assay, we examined the correlation between MALAT1 and miR-30a-5p. Dual-luciferase assay and western blotting suggested that Vimentin was a target of miR-30a-5p. A wound healing assay and transwell assays were employed to determine the effect of MALAT1 and miR-30a-5p on cell migration and invasion in HCC. Results Our data demonstrated that the levels of MALAT1 and Vimentin were upregulated in HCC tissues and that miR-30a-5p was a direct target of MALAT1. Silenced MALAT1 and overexpressed miR-30a-5p each inhibited cell migration and invasion. Additionally, dual-luciferase assay and western blotting demonstrated that MALAT1 could competitively sponge miR-30a-5p and thereby regulate Vimentin. Conclusion Our data suggest that MALAT1 acts as an oncogenic lncRNA that promotes HCC migration and invasion. Therefore, the MALAT1-miR-30a-5p-Vimentin axis is a potential therapeutic target and molecular biomarker in HCC.
机译：背景/目的肝细胞癌（HCC）具有很高的发病率和死亡率，被认为是全世界最普遍的癌症之一。长期的非编码RNA转移相关的肺腺癌转录本1（MALAT1）参与包括HCC在内的多种癌症。这项研究旨在探讨MALAT1在肝癌进展中的作用。方法采用RT-PCR和免疫组织化学方法检测肝癌组织及相对配对的邻近正常肝组织中MALAT1和波形蛋白的表达水平。使用生物信息学分析和双荧光素酶测定，我们检查了MALAT1和miR-30a-5p之间的相关性。双重荧光素酶测定和蛋白质印迹表明波形蛋白是miR-30a-5p的靶标。使用伤口愈合测定法和transwell测定法测定MALAT1和miR-30a-5p对肝癌中细胞迁移和侵袭的影响。结果我们的数据表明，HCC组织中MALAT1和波形蛋白的水平上调，而miR-30a-5p是MALAT1的直接靶标。沉默的MALAT1和过表达的miR-30a-5p均抑制细胞迁移和侵袭。此外，双重荧光素酶测定和蛋白质印迹证明，MALAT1可以竞争性地侵染miR-30a-5p，从而调节波形蛋白。结论我们的数据表明MALAT1可以作为致癌lncRNA来促进HCC迁移和侵袭。因此，MALAT1-miR-30a-5p-波形蛋白轴是肝癌的潜在治疗靶标和分子生物标志物。

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