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.

Hepatocellular carcinoma (HCC) is one of the malignant cancers with high incidence and mortality rates worldwide. RNA-binding protein eukaryotic initiation Factor 4A-III (eIF4AIII) 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 eIF4AIII 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 eIF4AIII participated in HCC. The results revealed that eIF4AIII was overexpressed in HCC. Lost-of-function assays found that eIF4AIII 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, eIF4AIII 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 eIF4AIII and miR-2113. Rescue assays verified that eIF4AIII 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 eIF4AIII in HCC, providing an optional therapy for HCC patients.

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