| Literature DB >> 26893711 |
Fang Ni1, Zhaohua Gui1, Qiang Guo1, Zhongqian Hu1, Xinyi Wang1, Danlei Chen1, Siying Wang1.
Abstract
An increasing number of studies have indicated that the deregulation of microRNAs (miRNAs) contributes to tumorigenesis and metastasis. In the present study, significant upregulation of miR-362-5p was identified in the breast cancer MDA-MB-231 and MCF7 cell lines compared with the control CCD-1095Sk cell line. The inhibition of miR-362-5p was demonstrated to significantly inhibit the cell proliferation, migration and invasion of human breast cancer MCF7 cells. In addition, the knockdown of miR-362-5p induced G1 arrest and promoted apoptosis in the breast cancer cells. Mechanistic investigations confirmed that the tumor suppressor gene CYLD is a direct target of miR-362-5p. The ectopic expression of miR-362-5p represses CYLD expression, whereas miR-362-5p inhibitor treatment induces CYLD protein expression and decreases NF-κB expression in the downstream signaling pathway. Thus, these findings may provide novel insights into the molecular mechanisms through which miR-362-5p regulates breast cancer cell proliferation, migration and invasion. This study also suggests that miR-362-5p may act as a novel potential therapeutic target for the treatment of breast cancer.Entities:
Keywords: breast cancer; invasion; miR-362-5p; migration; proliferation
Year: 2015 PMID: 26893711 PMCID: PMC4734047 DOI: 10.3892/ol.2015.3993
Source DB: PubMed Journal: Oncol Lett ISSN: 1792-1074 Impact factor: 2.967