MiR-509-3p Induces Apoptosis and Affects the Chemosensitivity of Cervical Cancer Cells by Targeting the RAC1/PAK1/LIMK1/Cofilin Pathway

Chemoresistance is one of the main factors treatment failure cervical cancer (CC). Here, we intended to discover role and mechanism miR-509-5p in paclitaxel chemoresistance CC cells. RT-PCR was conducted verify miR-509-3p expression. HCC94 C-33A paclitaxel-resistant cell models were constructed. Additionally, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay flow cytometry performed viability apoptosis cells after upregulating miR-509-3p. Besides, downstream target analyzed by bioinformatics, targeted relationship between RAC1 identified dual-luciferase reporter RNA immunoprecipitation (RIP) assay. Further, expression apoptotic proteins (Bcl2, Bax, Caspase3) RAC1/PAK1/LIMK1/Cofilin pathway monitored Western blot. The result showed that markedly inhibited promoted On other hand, distinctly downregulated (vs. normal cells). transfection mimics notably increased their sensitivity paclitaxel. Meanwhile, found as potential bioinformatics analysis. Moreover, RAC1/p21 (RAC1) activated kinase 1 (PAK1)/LIM (LIMK1)/Cofilin significantly cells, while overexpression inactivated this pathway. downregulation also partly reversed paclitaxel-resistance PAK1/LIMK1/Cofilin. All all, enhances chemosensitivity regulating