MicroRNA-200b Impacts Breast Cancer Cell Migration and Invasion by Regulating Ezrin-Radixin-Moesin.
BACKGROUND Ezrin-radixin-moesin (ERM) plays an important role in multiple links of tumors. It also involved in breast cancer invasion and metastasis, and might be a potential biomarker of breast cancer. Another study suggested that ERM expression was regulated directly by miR-200c, and had a critical role in miR-200c suppressing cell migration. This study aimed to investigate the effect of miR-200b on ERM expression in a breast cancer cell line and its influence on invasion and metastasis ability in vitro. MATERIAL AND METHODS Breast cancer cell lines MCF-7 and MDA-MB-231 with different metastatic potentials were selected as a model. MiR-200b overexpression or inhibition was achieved by Lipofectamine™ 2000-mediated miRNA transfection. RT-PCR was used to test miR-200b level, while Western blot was selected to detect ERM protein expression. Wound healing assay and Transwell assay were performed to determine cell migration and invasion ability. RESULTS RT-PCR revealed that miR-200b level in MDA-MB-231 was obviously lower than that in MCF-7, while Western blot analysis showed that ERM expression was significantly higher. MiR-200b inhibition by transfection in MCF-7 markedly decreased miR-200b level, elevated ERM expression, and enhanced cell migration and invasion. MiR-200b overexpression in MDA-MB-231 obviously increased miR-200b level, reduced ERM expression, and weakened cell migration and invasion. CONCLUSIONS MiR-200b participates in breast cancer cell migration and invasion through regulating ERM in MCF-7 and MDA-MB-231.
Department of Clinical Laboratory, Nantong Traditional Chinese Medicine Hospital, Nantong, Jiangsu, China (mainland).
Hong
H
Hong
Department of Clinical Laboratory, Nantong Traditional Chinese Medicine Hospital, Nantong, Jiangsu, China (mainland).
Haizhong
H
Yu
Department of Clinical Laboratory, Nantong Traditional Chinese Medicine Hospital, Nantong, Jiangsu, China (mainland).
Jianfen
J
Yuan
Department of Clinical Laboratory, Nantong Traditional Chinese Medicine Hospital, Nantong, Jiangsu, China (mainland).
Chunyan
C
Guo
Department of Clinical Laboratory, Nantong Traditional Chinese Medicine Hospital, Nantong, Jiangsu, China (mainland).
Hongyan
H
Cao
Department of Clinical Laboratory, Nantong Traditional Chinese Medicine Hospital, Nantong, Jiangsu, China (mainland).
Weibing
W
Li
Department of Clinical Laboratory, Nantong Tumor Hospital, Nantong, Jiangsu, China (mainland).
Chunhong
C
Xiao
D017311:Amlodipine / Q000378:metabolism; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics*; D049109:Cell Proliferation / Q000235:genetics; D004268:DNA-Binding Proteins / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D005260:Female; D006801:Humans; D061986:MCF-7 Cells; D035683:MicroRNAs / Q000008:administration & dosage / Q000096:biosynthesis / Q000235:genetics* / Q000378:metabolism; D009361:Neoplasm Invasiveness; D014157:Transcription Factors / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D014162:Transfection
D004268:DNA-Binding Proteins; C086680:ETV5 protein, human; C533896:MIRN200 microRNA, human; D035683:MicroRNAs; D014157:Transcription Factors; D017311:Amlodipine