title: [Effects of miR-106b expression on the proliferation of human hepatocellular carcinoma cells].
abstract: OBJECTIVE
  To investigate the effects of miR-106b expression on the proliferation of human hepatocellular carcinoma cells.
  
  
  METHODS
  Real-time PCR was used to detect the expression of miR-106b in human hepatocellular carcinoma (HCC) cell lines and normal liver epithelial THLE3 cells. Over-expression of miR-106b was transfected by miR-106b mimics, and inhibition of miR-106b expression was transfected by miR-106b inhibitors. The effects of miR-106b expression on the proliferation of HCC cells were detected by MTT, clone formation assay and anchorage-independent growth ability assay. Bromodeoxyuridine labeling and flow cytometry analysis were used to examine the effects of miR-106b expression on the cell cycle distribution of the HCC cells.
  
  
  RESULTS
  Compared with that in the normal liver epithelial THLE3 cells, the relative expression of miR-106b in HepG2, QGY-7703, BEL-7402, MHCC97H, HCCC-9810, Hep3B, MHCC97L and Huh7 cell lines were 5.37 ± 0.35, 8.45 ± 0.75, 19.22 ± 1.74, 11.93 ± 1.26, 17.03 ± 0.97, 4.19 ± 0.67, 7.94 ± 1.35 and 3.82 ± 0.87, respectively (P < 0.05 for all). Three days after transfection, the miR-106b over-expression was accelerated, while miR-106b inhibitor suppressed the proliferation of HCC cells. The numbers of clones formed were (4.13 ± 0.75) and (3.78 ± 0.47) times higher than that of control cells, and (147.73 ± 15.56) and (138.87 ± 15.58) clones in diameter >1.0 mm were formed by miR-106b-overexpressing cells. When the miR-106b expression was inhibited in the HepG2 and QGY-7703 cells, the clone numbers were (0.18 ± 0.05) and (0.24 ± 0.07) times of that in the controls, and the numbers of clones formed were (23.29 ± 7.14) and (20.60 ± 8.07) (P < 0.05 for all). The positive rates of BrdU labeled miR-106b-overexpressing HepG2 and QGY-7703 cells were (51.89 ± 4.91) % and (54.74 ± 6.10) %, those of the miR-106b-inhibited cells were (6.48 ± 3.15) % and (7.52 ± 2.03) %, significantly different from that in the control cells (P < 0.05 for all). The S phases were dramatically increased from 29.93% and 31.04% to 56.76% and 57.22% in the miR-106b-overexpressing HepG2 and QGY-7703 cells, while they were 19.43% and 19.92% in the miR-106b-inhibited HepG2 and QGY-7703 cells.
  
  
  CONCLUSIONS
  MiR-106b overexpression may promote the proliferation and metastasis of HCC cells. The mechanism of this effect may be related to promoting cells into S phase and inhibiting cell apoptosis.
authors.affiliation: Department of Interventional Radiology and Vascular Malformations, Guangzhou Women and Children's Medical Center, Guangzhou 510263, China. Email: gs1975@163.com.
authors.forename: Gang
authors.initials: G
authors.lastname: Shen
authors.forename: Hongyun
authors.initials: H
authors.lastname: Jia
authors.forename: Deji
authors.initials: D
authors.lastname: Chen
authors.forename: Jing
authors.initials: J
authors.lastname: Zhang
mesh_terms: D017209:Apoptosis; D006528:Carcinoma, Hepatocellular; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D035683:MicroRNAs / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D014162:Transfection
chemical_list: C542541:MIRN106 microRNA, human; D035683:MicroRNAs