X-J Zhu1, X Jin, L Dai, X Liu, Z Liu. 1. Department of Gastroenterology, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, China. zhuxiaojuan@njmu.edu.cn.
Abstract
OBJECTIVE: ATG14, as an autophagy-related protein, has been shown to be implicated in the progression of tumors by modulating cell autophagy. We aimed at exploring ATG14 level in hepatocellular carcinoma (HCC) and its possible molecular mechanism. PATIENTS AND METHODS: ATG14 levels in HCC tissues and cell lines were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and the relationship between ATG14 expression and clinical parameters was analyzed through clinical information analysis. The impacts of ATG14 on the proliferation and invasiveness of HCC cells were evaluated by performing Cell Counting Kit-8 (CCK-8) and transwell tests, respectively. We further explored the potential mechanism of ATG14 action using bioinformatics analysis and in vitro cell experiments. RESULTS: Our data showed that ATG14 levels were abnormally enhanced in HCC tissues and cell lines, which predicted a poor prognosis of HCC patients. Downregulation of ATG14 markedly blunted the proliferation and migratory capacities of HCC cells. Bioinformatics analysis suggested that XIST can regulate ATG14 by binding multiple miRNAs (miR-195-5p, miR-497-5p, miR-424-5p, and miR-16-5p). In addition, XIST promoted cell autophagy by elevating ATG14 expression, thereby providing possible mechanisms by which ATG14 and XIST could modulate the development of HCC. CONCLUSIONS: In summary, our data preliminary verified ATG14 levels were abnormally enhanced in HCC tissues and cell lines, which predicted a poor prognosis of HCC patients.
OBJECTIVE:ATG14, as an autophagy-related protein, has been shown to be implicated in the progression of tumors by modulating cell autophagy. We aimed at exploring ATG14 level in hepatocellular carcinoma (HCC) and its possible molecular mechanism. PATIENTS AND METHODS: ATG14 levels in HCC tissues and cell lines were examined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and the relationship between ATG14 expression and clinical parameters was analyzed through clinical information analysis. The impacts of ATG14 on the proliferation and invasiveness of HCC cells were evaluated by performing Cell Counting Kit-8 (CCK-8) and transwell tests, respectively. We further explored the potential mechanism of ATG14 action using bioinformatics analysis and in vitro cell experiments. RESULTS: Our data showed that ATG14 levels were abnormally enhanced in HCC tissues and cell lines, which predicted a poor prognosis of HCC patients. Downregulation of ATG14 markedly blunted the proliferation and migratory capacities of HCC cells. Bioinformatics analysis suggested that XIST can regulate ATG14 by binding multiple miRNAs (miR-195-5p, miR-497-5p, miR-424-5p, and miR-16-5p). In addition, XIST promoted cell autophagy by elevating ATG14 expression, thereby providing possible mechanisms by which ATG14 and XIST could modulate the development of HCC. CONCLUSIONS: In summary, our data preliminary verified ATG14 levels were abnormally enhanced in HCC tissues and cell lines, which predicted a poor prognosis of HCC patients.