Aim: Although aberrant miRNA expression has been documented, altered miR-101 expression in cervicalcancer and its carcinogenic effects and mechanisms remain unexplored. The aim of our study was to investigatethe role of miR-101 alteration in cervical carcinogenesis.
Methods: Expression of miR-101 was examined byquantitative real-time reverse transcriptase PCR (qRT-PCR) in Hela cells. After modulating miR-101 expressionusing miR-101 mimics, cell growth, apoptosis and proliferation, and migration were tested separately by MTT orflow cytometry and cell wound healing assay and protein expression was detected by qRT-PCR. The expressionof COX-2 in Hela cell was also examined by immunohistochemical staining and the correlation with miR-101expression was analysed.
Results: The miR-101 demonstrated significantly low expression in Hela cell. When wetransfected miR-101 mimics into Hela cells, the modulation of miR-101 expression remarkably influenced cellproliferation, cycling and apoptosis: 1) The expression of microRNA-101 tended to increase after transfection;2) Overexpression of miR-101 was able to promote cell apoptosis, the apoptosis rate being markedly higher(97.6%) than that seen pre-transfection (12.2%) (P <0.05); 3) The miR-101 negatively regulates cell migrationand invasion, scratch results being lower (42.7um±2um) than that observed pre-transfection (181.4 um±2 um);4) miRNA-101 inhibits the proliferation of Hela cells as well as the level of COX-2 protein, which was negativelycorrelated with miR-101 expression.
Conclusions: Overexpression of miR-101 has obvious inhibitory effects oncell proliferation, migration and invasion. Thus reduced miR-101 expression could participate in the developmentof cervical cancer at least partly through loss of inhibition of target gene COX-2, which probably occurs in arelative late phase of carcinogenesis. Our data suggest an important role of miR-101 in the molecular etiologyof cancer and indicate potential application of miR-101 in cancer therapy.