%A Li Bo*, Zhang Jiansheng, Li Jiaqi, Yang Yi, Zhang Hongxin, Mou Jiao %T Expression of MFF and its biological effects in hepatocellular carcinoma %0 Journal Article %D 2018 %J Journal of International Oncology %R 10.3760/cma.j.issn.1673-422X.2018.01.004 %P 16- %V 45 %N 1 %U {https://gjzlx.sdfmu.edu.cn/CN/abstract/article_10382.shtml} %8 2018-01-08 %X ObjectiveTo evaluate the expression of mitochondrial fission factor (MFF) and its biological effects in the progression of hepatocellular carcinoma (HCC). Methods①Quantitative realtime PCR (qPCR), Western blotting and immunohistochemistry analysis were used to detect the expression levels of MFF in HCC tumor tissues and cell lines. ②The effect of MFF knockdown on proliferation of HCC cells was analyzed by methyl thiazolyl tetrazolium (MTT) and colony formation assays in siCtrl, siMFF#1, siMFF#2 groups. ③The effect of MFF knockdown on apoptosis of HCC cells was analyzed by apoptosis assay with Annexin ⅤFITC and PI. Results①The MFF expression was higher in tumor tissues compared with tumoradjacent normal tissues ［mRNA level M(QR): 0.292(0.443) vs. 0.235(0.333), Z=-4.166, P＜0.001; protein level M(QR): 5.414 (4.545) vs. 3.120 (3.955), Z=-3.961， P＜0.001)］. The MFF expression was higher in HCC cell lines compared with normal liver cell line. ②RNA interferencemediated knockdown of MFF inhibited proliferation of HCC cells (siCtrl vs. siMFF#1: 5.29±0.34 vs. 3.34±0.37, P=0.014; siCtrl vs. siMFF#2: 5.29±0.34 vs. 3.09±0.40, P=0.010). RNA interferencemediated knockdown of MFF inhibited colony formation of HCC cells (siCtrl vs. siMFF#1: 95.35±21.20 vs. 37.56±10.61, P=0.003; siCtrl vs. siMFF#2: 95.35±21.20 vs. 41.23±10.82, P=0.004). ③RNA interferencemediated knockdown of MFF induced apoptosis of HCC cells (siCtrl vs. siMFF#1: 9.56%±1.70% vs. 20.08%±2.03%, P＜0.001; siCtrl vs. siMFF#2: 9.56%±1.70% vs. 21.14%±1.38%, P＜0.001). ConclusionMFF is overexpressed in HCC, which accelerates cell proliferation and suppresses apoptosis, indicating that MFF can serve as a potential oncogene and drug target in HCC treatment.