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MALAT1 promotes the proliferation and metastasis of gallbladder cancer cells by activating the ERK/MAPK pathway

机译:MALAT1通过激活ERK / MAPK途径促进胆囊癌细胞的增殖和转移

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摘要

Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA (lncRNA), is associated with metastasis and is an independent prognostic factor for lung cancer. Recent studies have demonstrated that MALAT1 plays an important role in other malignancies. However, little is known about the role of MALAT1 in gallbladder carcinoma (GBC), which is the most common cancer of the biliary tract and has an extremely poor prognosis. In this study, we focused on the expression, biological functions and mechanism of MALAT1 in GBC and found that MALAT1 was significantly upregulated in GBC tissues compared with corresponding non-cancerous tissues. Knockdown of MALAT1 in GBC cell lines using lentivirus-mediated RNA interference significantly inhibited the proliferation and metastasis of the GBC cells both in vitro and in vivo. Furthermore, ERK/MAPK pathway was found to be inactivated in the GBC cell lines after MALAT1 knockdown. These results indicated that MALAT1 might serve as an oncogenic lncRNA that promotes proliferation and metastasis of GBC and activates the ERK/MAPK pathway
机译:转移相关的肺腺癌转录本1(MALAT1)是一种长的非编码RNA(lncRNA),与转移相关,并且是肺癌的独立预后因素。最近的研究表明,MALAT1在其他恶性肿瘤中也起着重要作用。但是,关于MALAT1在胆囊癌(GBC)中的作用知之甚少,胆囊癌是胆道癌中最常见的一种,预后极差。在这项研究中,我们着眼于MALAT1在GBC中的表达,生物学功能和机制,发现与相应的非癌性组织相比,MALAT1在GBC组织中显着上调。使用慢病毒介导的RNA干扰在GBC细胞系中敲除MALAT1可以在体外和体内显着抑制GBC细胞的增殖和转移。此外,发现在敲除MALAT1后,GBC细胞系中的ERK / MAPK途径被灭活。这些结果表明,MALAT1可能作为致癌的lncRNA,可促进GBC的增殖和转移并激活ERK / MAPK途径。

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