OBJECTIVE: MicroRNAs (miRs) function as either oncogenes or tumor suppressors in the progression of various human cancers, including cervical cancer. This study aimed to explore the role of miR-212 in cervical cancer and the mechanisms underlying this role. PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (RT-PCR) and Western blot assays were used to determine the expression levels of miR-212 and TCF7L2 in the cervical cancer cells. Cell proliferation invasion was examined using BrdU assays and transwell, respectively. A bioinformatics analysis was used to predict targets, and a dual-luciferase reporter system was applied for validation. RESULTS: In our study, we demonstrated that miR-212 expression was significantly downregulated in cervical cancer tissues and cell lines. Moreover, the increased expression of miR-212 suppressed cell proliferation and invasion of cervical cancer cell lines in vitro. On the contrary, the decreased expression of miR-212 promoted cell proliferation and invasion of cervical cancer cell lines. Finally, the results of Western blot showed that overexpression of miR-212 dramatically suppressed the protein expression of TCF7L2. The knockdown of miR-212 showed the contrary effect. Luciferase reporter assay identified TCF7L2 as a novel direct target of miR-212. CONCLUSIONS: Our results revealed that miR-212 inhibited cervical cancer metastasis and progression by targeting TCF7L2 expression.
OBJECTIVE: MicroRNAs (miRs) function as either oncogenes or tumor suppressors in the progression of various humancancers, including cervical cancer. This study aimed to explore the role of miR-212 in cervical cancer and the mechanisms underlying this role. PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (RT-PCR) and Western blot assays were used to determine the expression levels of miR-212 and TCF7L2 in the cervical cancer cells. Cell proliferation invasion was examined using BrdU assays and transwell, respectively. A bioinformatics analysis was used to predict targets, and a dual-luciferase reporter system was applied for validation. RESULTS: In our study, we demonstrated that miR-212 expression was significantly downregulated in cervical cancer tissues and cell lines. Moreover, the increased expression of miR-212 suppressed cell proliferation and invasion of cervical cancer cell lines in vitro. On the contrary, the decreased expression of miR-212 promoted cell proliferation and invasion of cervical cancer cell lines. Finally, the results of Western blot showed that overexpression of miR-212 dramatically suppressed the protein expression of TCF7L2. The knockdown of miR-212 showed the contrary effect. Luciferase reporter assay identified TCF7L2 as a novel direct target of miR-212. CONCLUSIONS: Our results revealed that miR-212 inhibited cervical cancer metastasis and progression by targeting TCF7L2 expression.