MiR-144-3p-mediated dysregulation of EIF4G2 contributes to the development of hepatocellular carcinoma through the ERK pathway

Abstract Background Hepatocellular carcinoma (HCC) is one of the most common cancers with high incidence and mortality. However, underlying mechanisms HCC still remain unclear. Eukaryotic translation initiation factors (eIFs) have a substantial effect on tumor development. In this study, we were aimed to investigate role eukaryotic factor 4 gamma 2 (EIF4G2) in HCC. Methods Western blot (WB) 30 paired tissues tissue microarrays (TMAs) conducted by immunohistochemistry (IHC) 89 samples performed assess EIF4G2 expression. Clone formation, real-time cell analysis (RTCA), wound healing transwell assays adopted evaluate proliferation, migration invasion abilities. The function growth was assessed xenograft nude mouse model vivo. regulation miR-144-3p luciferase reporter assay WB. Results protein clearly upregulated tissues, expression closely related prognosis. silencing could inhibit metastasis vitro, suppress tumorigenesis vivo repressing ERK signaling pathway. results assays, WB IHC staining verified that negatively regulated miR-144. And re-expression partially reverse inhibiting miR-144 Conclusion summary, our study revealed development via activation We also found be suppressor Our investigations indicated might promising therapeutic target