Conclusion
Upregulation of miR-335-5p expression enhanced the cisplatin sensitivity of ovarian cancer cells through suppressing BCL2L2, suggesting the potential of miR-335-5p/BCL2L2 axis as a therapeutic target for the cisplatin resistance of patients with ovarian cancer.
Methods
Microarray analysis was used to determine differentially expressed microRNAs in primary and cisplatin-resistant A2780 cells. Cell function experiments were conducted to investigate the effect of miR-335-5p on the cisplatin sensitivity of A2780 cells. The targeted relationship between BCL2L2 mRNA and miR-335-5p was validated through luciferase assay. Tumor xenograft was performed to confirm the function of miR-335-5p in restoring the cisplatin sensitivity of the ovarian cancer cells.
Objective
Our study was designed to explore the association miR-335-5p and BCL2L2 and to investigate the influence of miR-335-5p/BCL2L2 axis on cisplatin-resistant ovarian cancer cells.
Results
MiR-335-5p was lowly expressed in cisplatin-resistant A2780 cells. Overexpression of miR-335-5p reduced cell survival and enhanced cisplatin-induced cell apoptosis. BCL2L2 mRNA was a target of miR-335-5p, and silencing of BCL2L2 showed the similar results on the cell viability as miR-335-5p overexpression.