miR-137 suppresses the invasion and procedure of EMT of human breast cancer cell line MCF-7 through targeting CtBP1

被引:27
|
作者
Han, Yong [1 ]
Bi, Yueyang [2 ]
Bi, Haiyang [3 ]
Diao, Caimei [4 ]
Zhang, Guoqiang [1 ]
Cheng, Kai [1 ]
Yang, Zhenlin [1 ]
机构
[1] Affiliated Hosp Binzhou Med Univ, Dept Breast & Thyroid Surg, Binzhou 256603, Shandong, Peoples R China
[2] Affiliated Hosp Binzhou Med Univ, Dept Resp Med, Binzhou 256603, Shandong, Peoples R China
[3] Jingqu Hosp Weihai City, Dept Gen Surg, Weihai 264200, Shandong, Peoples R China
[4] Peoples Hosp South Dist Qingdao, Dept Gynecol & Obstet, Qingdao 266000, Shandong, Peoples R China
来源
HUMAN CELL | 2016年 / 29卷 / 01期
基金
中国国家自然科学基金;
关键词
Breast cancer; miR-137; Metastasis; EMT; CtBP1; EPITHELIAL-MESENCHYMAL TRANSITION; GENE-REGULATION; MICRORNAS; CARCINOGENESIS; PROGRESSION; MELANOMA; PROTEIN; FOE;
D O I
10.1007/s13577-015-0124-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Distant metastasis is the predominant site of gastric cancer recurrence and the most common cause of death. Recently, accumulating evidence has established that aberrant epithelial-mesenchymal transition activation plays a crucial role in the genesis, invasion, and metastasis of various cancers, including breast cancer. In this paper, we found that miR-137, which has been reported to function as a tumor suppressor in a variety of cancers, could significantly suppress the migration and invasion of MCF-7 cells, which might be correlated with its suppressive effects on the EMT procedure. Upon transfection, the epithelial marker, E-cadherin, was up-regulated, and the mesenchymal markers, N-cadherin and Vimentin, were suppressed. Moreover, we also found that carboxyl-terminal binding protein 1 (CtBP1) was a putative target gene of miR-137 in MCF-7 cells, and might be involved in the suppressive effects, which might provide novel diagnostic and therapeutic options for human breast cancer in the future.
引用
收藏
页码:30 / 36
页数:7
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