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Eukaryotic elongation factor-1α 2 knockdown inhibits hepatocarcinogenesis by suppressing PI3K/Akt/NF-κb signaling

World Journal of Gastroenterology 2016年第16期22卷 4226-4237页

作者： Fu-Nan Qiu Yi Huang Dun-Yan Chen Feng Li Yan-An Wu Wen-bing Wu Xiao-Li Huang Provincial Clinical College Fujian Medical University Department of Hepatobiliary Surgery Fujian Provincial Hospital Department of Clinical Laboratory Fujian Provincial Hospital Department of Pathology Fujian Provincial Hospital

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 ***: 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 ***: 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 ***: eEF1A2, highly expressed in HCC, is a potential oncogene. Its silencing significantly decreases HCC tumorigenesis, likely by inhibiting PI3K/Akt/NF-κb signaling.

关键词： Hepatocellular carcinoma Carcinogenesis Eukaryotic elongation factor 1 alpha 2 Proliferation PI3K/Akt/NF-ba b signaling pathway

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