Abstract
miR-193b-3p was found to be downregulated and contributed to ovarian cancer (OC) progression. In the present study, we aimed to study the detailed role of miR-193b-3p in the development of OC and the underlying molecular mechanism. The results showed that miR-193b-3p was downregulated while PAK3 was upregulated in OC cells. Ectopic expression of miR-193b-3p and PAK3 knockdown repressed cell proliferation, promoted paclitaxel-induced cytotoxicity, and reinforced paclitaxel-mediated caspase-3 activity increase in OC cells. Notably, miR-193b-3p was identified to directly target PAK3 and suppressed PAK3 expression. Moreover, enforced expression of PAK3 partially overturned the effects of miR-193b-3p on OC cell proliferation and paclitaxel sensitivity. In conclusion, miR-193b-3p possessed anti-tumor activity in OC through inhibiting cell proliferation and enhancing paclitaxel sensitivity by targeting PAK3. Therefore, our study suggested that the miR-193b-3p/PAK3 axis might be a potential novel therapeutic target for OC.
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