miR-125b inhibited epithelialal–mesenchymal transition of triple-negative breast cancer by targeting MAP2K7

Liquan Hong,1 Feng Pan,1 Huifen Jiang,2 Lahong Zhang,1 Yuhua Liu,1 Chengsong Cai,1 Chunzhen Hua,3 Xian Luo,1 Jinhua Sun,4 Zhaojun Chen1 1Department of Clinical Laboratory, Affiliated Hospital of Hangzhou Normal University, 2Zhejiang Provincial Tumor Hospital, 3Zhejiang Provincial Children’s Hospital, 4Technology Department, Hangzhou Joingenome Diagnostics, Hangzhou, Zhejiang Province, People’s Republic of China Abstract: MicroRNAs (miRNAs) play important roles in diverse biological processes and are emerging as key regulators of tumorigenesis and tumor progression. Among the differentially expressed miRNAs in breast cancer, miR-125b was revealed to be deregulated and associated with poor prognosis and chemoresistance in triple-negative breast cancer (TNBC), but the mechanism is still unknown. In our study, we showed downregulated expression of miR-125b in TNBC tissues and decreased migration and invasion in miR-125b-expressing Hs578T cells. MAP2K7 was then detected to be a novel target of miR-125b, and downregulation of MAP2K7 by miR-125b was similar to transient knockdown of MAP2K7 which hindered epithelial–­mesenchymal transition (EMT) of Hs578T cells. Upregulation of MAP2K7 in miR-125b-overexpressing Hs578T cells partly rescued the migration and invasion suppression of miR-125b. Furthermore, MAP2K7 was overexpressed in TNBC samples compared with normal tissues and negatively correlated with miR-125b expression. In light of these findings, miR-125b emerged as a tumor suppressor in TNBC by targeting MAP2K7 to inhibit EMT. Keywords: miR-125b, MAP2K7, TNBC, Hs578T, EMT