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首页> 外文期刊>Journal of cellular physiology. >Eukaryotic initiation Factor 4AIII facilitates hepatocellular carcinoma cell proliferation, migration, and epithelial-mesenchymal transition process via antagonistically binding to WD repeat domain 66 with miRNA-2113
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Eukaryotic initiation Factor 4AIII facilitates hepatocellular carcinoma cell proliferation, migration, and epithelial-mesenchymal transition process via antagonistically binding to WD repeat domain 66 with miRNA-2113

机译：真核起始因子4哎便利肝癌细胞增殖,移民和epithelial-mesenchymal过渡通过反对地绑定到WD重复过程域66年microrna - 2113

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摘要

Hepatocellular carcinoma (HCC) is one of the malignant cancers with high incidence and mortality rates worldwide. RNA-binding protein eukaryotic initiation Factor 4A-III (elF4AIII) is a carcinogene in the biological process of tumors and microRNA (miRNA)-2113 has rarely been studied in cancers, not to mention in HCC. The regulation mechanism between elF4AIII and miR-2113 involved in HCC is yet to be explored. The purpose of this research is to probe the function role and associated underlying mechanism of elF4AIII participated in HCC. The results revealed that elF4AIII was overexpressed in HCC. Lost-of-function assays found that elF4AIII knockdown, WD (Trp-Asp [tryptophan and asparaginic acid]) repeat domain 66 (WDR66) silence or miR-2113 promotion repressed cell proliferation, migration, and epithelial-mesenchymal transition (EMT) process in HCC. Furthermore, elF4AIII could interact with WDR66 and further stabilize WDR66 messenger RNA. In addition, WDR66 was a target gene of miR-2113. Besides, WDR66 was antagonistically regulated by elF4AIII and miR-2113. Rescue assays verified that elF4AIII promoted HCC cell proliferation, migration, and EMT process via antagonistically binding to WDR66 with miR-2113. Taken together, these findings indicated an important role and a novel mechanism of elF4AIII in HCC, providing an optional therapy for HCC patients.
机译：肝细胞癌(HCC)是其中一个恶性肿瘤发病率和高全球死亡率。真核起始因子4 a-iii (elF4AIII)致癌基因在肿瘤的生物学过程和微(microRNA) -2113年很少被研究在癌症,更不用说在肝细胞癌。机制elF4AIII和mir - 2113之间在肝癌仍有待探索。研究调查的角色和功能相关elF4AIII的潜在机制参与肝细胞癌。elF4AIII在肝细胞中。Lost-of-function化验发现elF4AIII击倒,WD (Trp-Asp[色氨酸和天冬氨酸)重复域66 (WDR66)沉默或者mir - 2113促销压抑的细胞增殖、迁移和epithelial-mesenchymal过渡(EMT)过程在肝细胞癌。WDR66,进一步稳定WDR66信使RNA。此外,WDR66 mir - 2113的目标基因。此外,WDR66反对地受了elF4AIII和mir - 2113。elF4AIII促进肝癌细胞增殖,通过反对地迁移,EMT过程绑定WDR66 mir - 2113。这些发现表明,一个重要的角色小说在HCC elF4AIII机制,提供一个可选的治疗肝癌的病人。

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