摘要
AIM: To assess the impact of eukaryotic elongation factor 1 alpha 2 (eEF1A2) on hepatocellular carcinoma (HCC) cell proliferation, apoptosis, migration and invasion, and determine the underlying mechanisms.METHODS: eEF1A2 levels were detected in 62 HCC tissue samples and paired pericarcinomatous specimens, and the human HCC cell lines SK-HEP-1, HepG2 and BEF-7402, by real-time PCR and immunohistochemistry. Experimental groups included eEF1A2 silencing in BEL-7402 cells with lentivirus eEF1A2-shRNA (KD group) and eEF1A2 overexpression in SK-HEP-1 cells with eEF1A2 plasmid (OE group). Non-transfected cells (control group) and lentivirus-based empty vector transfected cells (NC group) were considered control groups. Cell proliferation (MTT and colony formation assays), apoptosis (Annexin V-APC assay), cell cycle (DNA ploidy assay), and migration and invasion (Transwell assays) were assessed. Protein levels of PI3K/Akt/NF-κB signaling effectors were evaluated by Western blot.RESULTS: eEF1A2 mRNA and protein levels were significantly higher in HCC cancer tissue samples than in paired pericarcinomatous and normal specimens. SK-HEP-1 cells showed lower eEF1A2 mRNA levels; HepG2 and BEL-7402 cells showed higher eEF1A2 mRNA levels, with BEL-7402 cells displaying the highest amount. Efficient eEF1A2 silencing resulted in reduced cell proliferation, migration and invasion, increased apoptosis, and induced cell cycle arrest. The PI3K/Akt/NF-κB signaling pathway was notably inhibited. Inversely, eEF1A2 overexpression resulted in promoted cell proliferation, migration and invasion.CONCLUSION: eEF1A2, highly expressed in HCC, is a potential oncogene. Its silencing significantly decreases HCC tumorigenesis, likely by inhibiting PI3K/Akt/NF-κB signaling.
AIM: To assess the impact of eukaryotic elongation factor 1 alpha 2(e EF1A2) on hepatocellular carcinoma(HCC) cell proliferation, apoptosis, migration and invasion, and determine the underlying mechanisms.METHODS: e EF1A2 levels were detected in 62 HCC tissue samples and paired pericarcinomatous specimens, and the human HCC cell lines SK-HEP-1, Hep G2 and BEF-7402, by real-time PCR and immunohistochemistry. Experimental groups included e EF1A2 silencing in BEL-7402 cells with lentivirus e EF1A2-sh RNA(KD group) and e EF1A2 overexpression in SK-HEP-1 cells with e EF1A2 plasmid(OE group). Non-transfected cells(control group) and lentivirusbased empty vector transfected cells(NC group) were considered control groups. Cell proliferation(MTT and colony formation assays), apoptosis(Annexin V-APC assay), cell cycle(DNA ploidy assay), and migration and invasion(Transwell assays) were assessed. Protein levels of PI3K/Akt/NF-κB signaling effectors were evaluated by Western blot.RESULTS: e EF1A2 m RNA and protein levels were significantly higher in HCC cancer tissue samples than in paired pericarcinomatous and normal specimens. SK-HEP-1 cells showed lower e EF1A2 m RNA levels; Hep G2 and BEL-7402 cells showed higher e EF1A2 m RNA levels, with BEL-7402 cells displaying the highest amount. Efficient e EF1A2 silencing resulted in reduced cell proliferation, migration and invasion, increased apoptosis, and induced cell cycle arrest. The PI3K/Akt/NF-κB signaling pathway was notably inhibited. Inversely, e EF1A2 overexpression resulted in promoted cell proliferation, migration and invasion.CONCLUSION: e EF1A2, highly expressed in HCC, is a potential oncogene. Its silencing significantly decreases HCC tumorigenesis, likely by inhibiting PI3K/Akt/NF-κB signaling.
基金
Supported by the Middle-Young Age Backbone Talent Cultivation Program of Fujian Health System,No.2013-ZQNJC-2
Key Projects of Science and Technology Plan of Fujian Province,No.2014Y0009
