期刊
CANCER CELL INTERNATIONAL
卷 17, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s12935-017-0383-0
关键词
MiR-32; Breast cancer; FBXW7; Proliferation; Apoptosis
类别
资金
- China Postdoctoral Science Foundation [2016M602487]
- Program of the Pearl River Young Talents of Science and Technology in Guangzhou, China [2013J2200042]
- Natural Science Foundation of Guangdong Province, China [S2012010009404]
Background: MicroRNAs are a class of small non-coding RNAs that are involved in many important physiological and pathological processes by regulating gene expression negatively. The purpose of this study was to investigate the effect of miR-32 on cell proliferation, migration and apoptosis and to determine the functional connection between miR-32 and FBXW7 in breast cancer. Methods: In this study, quantitative RT-PCR was used to evaluate the expression levels of miR-32 in 27 breast cancer tissues, adjacent normal breast tissues and human breast cancer cell lines. The biological functions of miR-32 in MCF-7 breast cancer cells were determined by cell proliferation, apoptosis assays and wound-healing assays. In addition, the regulation of FBXW7 by miR-32 was assessed by qRT-PCR, Western blot and luciferase reporter assays. Results: MiR-32 was frequently overexpressed in breast cancer tissue samples and cell lines as was demonstrated by qRT-PCR. Moreover, the up-regulation of miR-32 suppressed apoptosis and promoted proliferation and migration, whereas down-regulation of miR-32 showed an opposite effect. Dual-luciferase reporter assays showed that miR32 binds to the 3'-untranslated region of FBXW7, suggesting that FBXW7 is a direct target of miR-32. Western blot analysis showed that over-expression of miR-32 reduced FBXW7 protein level. Furthermore, an inverse correlation was found between the expressions of miR-32 and FBXW7 mRNA levels in breast cancer tissues. Knockdown of FBXW7 promoted proliferation and motility and suppressed apoptosis in MCF-7 cells. Conclusions: Taken together, the present study suggests that miR-32 promotes proliferation and motility and suppresses apoptosis of breast cancer cells through targeting FBXW7.
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