Abstract: Objective：To investigate the role of microRNA-10b in the cervical carcinoma and explore its possible mechanism. Methods：The expression levels of microRNA-10b in cervical carcinoma cell lines and the normal cervical epithelial cells were detected by the real-time polymerase chain reaction (real-time PCR). The microRNA-10b mimics/NC was transfected into the Caski cells and the microRNA-10b inhibitor/NC inhibitor was transfected into the HeLa cells by the liposome. The Transwell assay and wound-healing assay were used to determine the effects of microRNA-10b on the invasion and migration ability in the Caski and HeLa cells. The mRNA and protein levels of insulin-like growth factor 1 receptor (IGF-1R) were analyzed by the real-time PCR and the Western blotting assay, respectively. Luciferase reporter assay was applied to detect the regulatory mechanism of microRNA-10b in the IGF-1R gene. Results：The expression levels of microRNA-10b in the cervical carcinoma cell lines were much lower than those in the normal cervical epithelial cells (P＜0.05). The up-regulation of microRNA-10b could decrease the invasion and migration ability of Caski cells (P＜0.05), and inhibit the mRNA and protein levels of IGF-1R (P＜0.05), while the downregulation of microRNA-10b could increase the invasion and migration ability of HeLa cells (P＜0.05), and increase the mRNA and protein levels of IGF-1R (P＜0.05). Besides, the up-regulation of microRNA-10b could decrease the luciferase activity of the reporter vector (containing the 5'untranslated region of IGF-1R gene) in the HEK-293T cells (P＜0.05). Conclusions：In cervical carcinoma cells, microRNA-10b could inhibit the cell invasion and migration capability, which may be the result of the down-regulation of IGF-1R gene.

Key words: MicroRNAs, Uterine cervical neoplasms, Neoplasm invasiveness, Cell movement