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首頁> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Hepatitis B virus X protein (HBx)-related long noncoding RNA (lncRNA) down-regulated expression by HBx (Dreh) inhibits hepatocellular carcinoma metastasis by targeting the intermediate filament protein vimentin
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Hepatitis B virus X protein (HBx)-related long noncoding RNA (lncRNA) down-regulated expression by HBx (Dreh) inhibits hepatocellular carcinoma metastasis by targeting the intermediate filament protein vimentin

機譯：乙肝病毒X蛋白（HBx）相關(guān)的長非編碼RNA（lncRNA）被HBx（Dreh）下調(diào)的表達通過靶向中間絲蛋白波形蛋白抑制肝癌的轉(zhuǎn)移

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The hepatitis B virus X protein (HBx) has been implicated as an oncogene in both epigenetic modifications and genetic regulation during hepatocarcinogenesis, but the underlying mechanisms are not entirely clear. Long noncoding RNAs (lncRNAs), which regulate gene expression with little or no protein-coding capacity, are involved in diverse biological processes and in carcinogenesis. We asked whether HBx could promote hepatocellular carcinoma (HCC) by regulating the expression of lncRNAs. In this study we investigated the alteration in expression of lncRNAs induced by HBx using microarrays and real-time quantitative polymerase chain reaction (PCR). Our results indicate that HBx transgenic mice have a specific profile of liver lncRNAs compared with wildtype mice. We identified an lncRNA, down-regulated expression by HBx (termed lncRNA-Dreh), which can inhibit HCC growth and metastasis in vitro and in vivo, act as a tumor suppressor in the development of hepatitis B virus (HBV)-HCC. LncRNA-Dreh could combine with the intermediate filament protein vimentin and repress its expression, and thus further change the normal cytoskeleton structure to inhibit tumor metastasis. We also identified a human ortholog RNA of Dreh (hDREH) and found that its expression level was frequently down-regulated in HBV-related HCC tissues in comparison with the adjacent noncancerous hepatic tissues, and its decrement significantly correlated with poor survival of HCC patients. Conclusion: These findings support a role of lncRNA-Dreh in tumor suppression and survival prediction in HCC patients. This discovery contributes to a better understanding of the importance of the deregulated lncRNAs by HBx in HCC and provides a rationale for the potential development of lncRNA-based targeted approaches for the treatment of HBV-related HCC. (HEPATOLOGY 2013)
機譯：乙型肝炎病毒X蛋白（HBx）已被認為是癌基因，參與肝癌發(fā)生過程中的表觀遺傳修飾和遺傳調(diào)控，但其潛在機制尚不完全清楚。長的非編碼RNA（lncRNA）調(diào)節(jié)基因表達時幾乎沒有或沒有蛋白質(zhì)編碼能力，它們參與多種生物學過程和致癌作用。我們詢問HBx是否可以通過調(diào)節(jié)lncRNA的表達來促進肝細胞癌（HCC）。在這項研究中，我們使用微陣列和實時定量聚合酶鏈反應(yīng)（PCR）研究了HBx誘導(dǎo)的lncRNA表達的變化。我們的結(jié)果表明，與野生型小鼠相比，HBx轉(zhuǎn)基因小鼠具有肝臟lncRNA的特異性特征。我們鑒定了一個lncRNA，被HBx下調(diào)表達（稱為lncRNA-Dreh），它可以在體外和體內(nèi)抑制HCC的生長和轉(zhuǎn)移，在乙型肝炎病毒（HBV）-HCC的發(fā)展中起著抑癌作用。 LncRNA-Dreh可與中間絲蛋白波形蛋白結(jié)合，并抑制其表達，從而進一步改變正常細胞骨架結(jié)構(gòu)，從而抑制腫瘤轉(zhuǎn)移。我們還鑒定了Dreh的人類直系同源RNA（hDREH），發(fā)現(xiàn)與鄰近的非癌性肝組織相比，其表達水平在HBV相關(guān)的HCC組織中經(jīng)常被下調(diào)，并且其減少與HCC患者的不良生存率顯著相關(guān)。結(jié)論：這些發(fā)現(xiàn)支持lncRNA-Dreh在HCC患者的腫瘤抑制和生存預(yù)測中的作用。這一發(fā)現(xiàn)有助于更好地了解HBx在HCC中對lncRNA的調(diào)節(jié)作用，并為潛在開發(fā)基于lncRNA的靶向方法治療HBV相關(guān)HCC提供了理論依據(jù)。 （2013年肝?。?

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