MicroRNA-155 regulates the proliferation and metastasis of human breast cancers by targeting MAPK7

被引:0
|
作者
Liu, Jian-Hua [1 ]
Yang, Yong [1 ]
Song, Qi [1 ]
Li, Jie-Bao [1 ]
机构
[1] Wuhan Chinese & Western Med Hosp, Dept Breast & Thyroid Surg, Wuhan Hosp 1, 215 Zhongshan Ave, Qiaokou Dist 430022, Hubei, Peoples R China
来源
JOURNAL OF BUON | 2019年 / 24卷 / 03期
关键词
microRNA; proliferation; apoptosis; cell cycle; CELL INVASION; MIGRATION; EPIDEMIOLOGY; EXPRESSION; APOPTOSIS; MIRNAS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Purpose: Breast cancer causes significant mortality in women world over. The lack of efficient and reliable biomarkers and therapeutic targets impedes the treatment of breast cancer. Herein, the role and therapeutic potential of miR-155 was investigated in different breast cancer cell lines . Methods: Cell viability was determined by WST-1 and colony formation assays. Transfections were performed by Lipofectamine 2000 reagent. Cell cycle analysis was carried out by flow cytometry and apoptosis was detected by AO (acridine orange)/EB (ethidium bromide) staining. Cell migration and cell invasion were determined by wound healing assay. RNA and protein expressions were determined by qRT-PCR and western blotting, respectively. Results: miR-155 was significantly upregulated in all the breast cancer cells. Suppression of miR-155 in SK-BR-3 cells inhibited the growth and colony formation. The inhibition of SK-BR-3 cell proliferation was found to trigger apoptotic cell death and cell cycle arrest. Induction of apoptosis was also accompanied with enhancement of cytochrome c, Bax caspase 3, 8 and 9 and inhibition of Bcl-2. Besides, suppression of miR-155 resulted in the decrease of cell migration and invasion. Bioinformatic analysis revealed MAPK7 to be the potential target of miR-155. The MAPK7 expression was also upregulated in all the breast cancer cells and suppression of miR-155 resulted in its downregulation. Conclusion: Taken together, miR-155 may prove essential in the management of breast cancer.
引用
收藏
页码:1075 / 1080
页数:6
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