STAT3 regulated <i>miR-216a</i> promotes ovarian cancer proliferation and cisplatin resistance

Abstract

Cisplatin is the first-line treatment for ovarian cancer. However, the clinical outcome of cisplatin treatment in ovarian cancer is hindered by cancer resistance. Here we aim to explore the role and mechanism of <i>miR-216a</i> in the cisplatin resistance of ovarian cancer. The effects of <i>miR-216a</i> overexpression and inhibition on ovarian cell proliferation, colony formation, and cisplatin resistance were investigated by MTT assay and soft agar colony formation assay. Bioinformatics analyses using TargetScan and rVista, qPCR, and luciferase assay were also used to explore and verify downstream effectors and regulators of <i>miR-216a</i> Proliferation, colony formation, and cisplatin resistance of ovarian cancer cells are promoted by <i>miR-216a</i> overexpression but inhibited by <i>miR-216a</i> inhibition. PTEN is a direct target of miR-216a and PTEN expression antagonizes the tumor-promoting function of <i>miR-216a</i> STAT3 is a regulator of <i>miR-216a</i>, and PTEN is also regulated by STAT3. <i>miR-216a</i> up-regulation is associated with cisplatin resistance in ovarian cancer and this effect is mediated by PTEN. STAT3 is a regulator of <i>miR-216a</i> Strategies that inhibit <i>miR-216a</i> is a potential strategy for overcoming the cisplatin resistance in ovarian cancer.