The exact expression profile and potential involvement of miR-625-5p in the tumor biology of cervical carcinoma are still elusive. In this study, we aimed to analyze the expression status and possible involvements of miR-625-5p in both clinical tissue samples and cell culture of cervical carcinoma. The relative expression levels of miR-625-5p and NF-κB transcript were determined by real-time polymerase chain reaction. Cell proliferation was measured using Cell Counting Kit-8. The protein levels of Cyclin D1, CDK4, NF-κB, and GAPDH were examined by Western blotting. The regulatory effects of miR-625-5p on NF-κB and MALAT1 were interrogated by luciferase reporter assay. We demonstrated that miR-625-5p was downregulated and predicted better survival in cervical carcinoma. Ectopic over-expression of miR-625-5p inhibited cell growth via targeting NF-κB. We further identified MALAT1 as the competitive endogenous long non-coding RNA for miR-625-5p, and over-expression of MALAT1 attenuated the inhibitory effect of miR-625-5p on NF-κB signaling in cervical carcinoma. Our study characterized the suppressive expression of miR-625-5p in cervical carcinoma and unraveled the importance of MALAT1/miR-625-5p/NF-κB signaling in this disease.
Keywords: Cervical carcinoma; Long non-coding RNA; MALAT1; NF-κB; miR-625-5p.