MiR-26a Inhibits Proliferation and Migration of Breast Cancer through Repression of MCL-1

被引:61
作者
Gao, Jie [1 ,3 ]
Li, Laisheng [2 ,3 ]
Wu, Minqing [1 ,3 ]
Liu, Min [2 ]
Xie, Xinhua [1 ,3 ]
Guo, Jiaoli [1 ,3 ]
Tang, Hailin [1 ,3 ]
Xie, Xiaoming [1 ,3 ]
机构
[1] Sun Yat Sen Univ, Ctr Canc, Dept Breast Oncol, Guangzhou 510275, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Affiliated Hosp 1, Dept Lab Med, Guangzhou 510275, Guangdong, Peoples R China
[3] Sun Yat Sen Univ, Ctr Canc, State Key Lab Oncol South China, Guangzhou 510275, Guangdong, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
PACLITAXEL-RESISTANCE; MICRORNA EXPRESSION; IN-VITRO; CELLS; METASTASIS; CARCINOGENESIS; CARCINOMA; APOPTOSIS; SURVIVAL; TARGETS;
D O I
10.1371/journal.pone.0065138
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
070301 [无机化学]; 070403 [天体物理学]; 070507 [自然资源与国土空间规划学]; 090105 [作物生产系统与生态工程];
摘要
Breast cancer is the most commonly malignancies in women. MicroRNAs are a family of small non-coding RNAs 18-25 nucleotides in length that post-transcriptionally modulate gene expression. MiR-26a has been reported as a tumor suppressor microRNA in breast cancer, which is attributed mainly to targeting of MTDH and EZH2, however, the expression profile and therapeutic potential of miR-26a is still unclear. Here we demonstrate that miR-26a is down-regulated in breast cancer cells and clinical specimens and its modulation in breast cancer cells regulates cell proliferation, colony formation, migration and apoptosis. MCL-1, an anti-apoptotic member of the Bcl-2 family, as novel targets of miR-26a was found to be in reverse correlation with ectopic expression of miR-26a and knockdown of MCL-1 phenocopied the effect of miR-26a in breast cancer cell lines. It was further explored that miR-26a increased sensitivity of breast cancer cells to paclitaxel in which MCL-1 was involved. Thus, miR-26a impacts on cell proliferation and migration of breast cancer by regulating several carcinogenesis-related processes, including a novel mechanism involving the targeting of MCL-1.
引用
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页数:10
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