作者: L.L. Zhou , J.L. Dong , G. Huang , Z.L. Sun , J. Wu
DOI: 10.1590/1414-431X20175891
关键词:
摘要: Abstract This study aimed to investigate the function and mechanism of microRNA-143 (miR-143) in occurrence development ofbreast cancer (BC). A total 30 BC tissues, corresponding noncancerous 10 normal control (NC) breast tissueswere obtained detect levels miR-143, extracellular signal-regulated kinase 5 (ERK5) mitogen-activated protein 3kinase 7 (MAP3K7) using RT-qPCR, western blotting or immunohistochemistry. The correlation miR-143 with ERK5 orMAP3K7 was evaluated Pearson analysis. MCF-7 cells were transiently transfected mimic,miR-143 inhibitor, mimic/inhibitor + si-ERK5, si-MAP3K7 si-cyclin D1. Then, cell growth by MTTassay expressions phospho-ERK5 (p-ERK5), ERK5, p-MAP3K7, MAP3K7 cyclin D1 detected westernblotting. Results showed that, compared tissues NC level decreased, whilep-ERK5, p-MAP3K7 increased (all Po0.01). wasnegatively correlated mRNA (r=–4.231 r=–4.280, In addition, up-regulated significantly decreased p-ERK5, Po0.01), as well cellviability Po0.05) while effect down-regulated opposite. conclusion, both ERK5and may be target genes miR-143. Increased expression can inhibit growth, which beassociated BC.Key words: Extracellular 5; Mitogen-activated 3 7; miRNA-143; Breast cancer; Cyclin