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Biochem Biophys Res Commun. 2016 Jan 1;469(1):55-61. doi: 10.1016/j.bbrc.2015.11.071. Epub 2015 Nov 22.

Arsenic trioxide suppresses cell growth and migration via inhibition of miR-27a in breast cancer cells.

Author information

1
Department of Medical Imaging, Bengbu Medical College, Anhui, 233030, China.
2
Research Center of Clinical Laboratory Science, Bengbu Medical College, Anhui, 233030, China.
3
Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui, 233030, China.
4
Department of Surgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, 519000, China.
5
Department of Anesthesiology, Shenzhen Baoan Hospital Affiliated to Southern Medical University, Guangdong, 518100, China. Electronic address: chenjianyan@yahoo.com.
6
Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui, 233030, China; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, 02215, MA, USA. Electronic address: zwang6@bidmc.harvard.edu.
7
Department of Biochemistry and Molecular Biology, Bengbu Medical College, Anhui, 233030, China. Electronic address: xiajunbbmc@126.com.

Abstract

Accumulating evidence has demonstrated that arsenic trioxide (ATO) exhibits its anti-cancer activities in a variety of human malignancies. Recent studies have revealed that ATO regulated multiple microRNAs (miRNAs) in human cancers. However, the exact mechanism of ATO-mediated tumor suppressive function has not been fully elucidated. In the present study, we explore whether ATO governed oncogenic miR-27a in breast cancer cells by multiple methods such as MTT assay, RT-PCR, Wound healing assay, Western blotting analysis, migration, Transwell invasion assay, and transfection. Our results showed that ATO inhibited cell growth, migration, invasion, and induced cell apoptosis in breast cancer cells. Further molecular analysis dissected that ATO inhibited miR-27a expression in breast cancer cells. Moreover, inhibition of miR-27a suppressed cell growth, migration, invasion, and trigged cell apoptosis, whereas overexpression of miR-27a enhanced cell growth, motility, and inhibited apoptosis in breast cancer cells. Notably, we found that miR-27a inhibitor treatment potentiates ATO-induced breast cancer cell growth inhibition, apoptosis and motility inhibition. However, overexpression of miR-27a partly abrogated ATO-mediated anti-tumor activity. Our findings provide a novel anti-tumor mechanism of ATO involved in miR-27a for the treatment of breast cancer.

KEYWORDS:

Apoptosis; Arsenic trioxide; Breast cancer; Cell growth; miR-27a

PMID:
26592661
DOI:
10.1016/j.bbrc.2015.11.071
[Indexed for MEDLINE]

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