Abstract
Objective To evaluate the expression of mitochondrial fission factor (MFF) and its biolo-gical effects in the progression of hepatocellular carcinoma (HCC). Methods ①Quantitative 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. Results ①The 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). Conclusion MFF 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. Key words: Liver neoplasms; Cell proliferation; Apoptosis; Mitochondrial fission factor
Published Version
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