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MiR-142-3p functions as a tumor suppressor by targeting RAC1/PAK1 pathway in breast cancer
Authors:Tao Xu  Bang-Shun He  Bei Pan  Yu-Qin Pan  Hui-Ling Sun  Xiang-Xiang Liu  Xue-Ni Xu  Xiao-Xiang Chen  Kai-Xuan Zeng  Mu Xu  Shu-Kui Wang
Affiliation:1. General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, China;2. General Clinical Research Center, Nanjing First Hospital, Nanjing Medical University, Nanjing, China

Medical College, Southeast University, Nanjing, China

Abstract:MicroRNA-142-3p (miR-142-3p) was previously investigated in various cancers, whereas, it's role in breast cancer (BC) remains far from understood. In this study, we found that miR-142-3p was markedly decreased both in cell lines and BC tumor tissues. Elevated miR-142-3p expression suppressed growth and metastasis of BC cell lines via gain-of-function assay in vitro and in vivo. Mechanistically, miR-142-3p could regulate the ras-related C3 botulinum toxin substrate 1 (RAC1) expression in protein level, which simultaneously suppressed the epithelial-to-mesenchymal transition related protein levels and the activity of PAK1 phosphorylation, respectively. In addition, rescue experiments revealed RAC1 overexpression could reverse tumor-suppressive role of miR-142-3p. Our results showed miR-142-3p could function as a tumor suppressor via targeting RAC1/PAK1 pathway in BC, suggesting a potent therapeutic target for BC treatment.
Keywords:breast cancer  miR-142-3p  PAK1  RAC1
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