Literature DB >> 26998102

MicroRNA-524-5p suppresses the growth and invasive abilities of gastric cancer cells.

Guang-Hui Liu1, Yuan-Hua Liu1, Zhen Yang1, A-Li Zhu1, Chun-Lin Zhao1.   

Abstract

Previous studies have demonstrated that microRNAs (miRNAs) are associated with tumor development and progression. miRNA-524-5p (miR-524-5p) has been reported to be involved in the development and progression of several types of cancer, but its role in gastric cancer has not been fully elucidated to date. Therefore, the aim of the present study was to investigate the expression levels and function of miR-524-5p in human gastric cancer. The expression levels of miR-524-5p were assessed in gastric cancer specimens and cell lines, including MKN-45, SGC-7901 and MGC-803 cell lines and gastric epithelial mucosa GES-1 cells, using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell proliferation and cell apoptosis assays and invasion analysis in gastric cancer cell lines were performed to evaluate the effects of miR-524-5p on gastric cancer cells in vitro. The expression levels of matrix metallopeptidase (MMP)-2 and MMP-9 were determined by RT-qPCR and western blot analysis. The expression of miR-524-5p was significantly decreased in gastric cancer tissues and cell lines. Additionally, the results of the in vitro experiments demonstrated that overexpression of miR-524-5p inhibited cell proliferation and invasion, and promoted cell apoptosis in gastric cancer cells. Human gastric cancer SGC-7901 and MGC-803 cell lines transfected with miR-524-5p exhibited reduced expression levels of MMP-2 and MMP-9. Taken together, the results of the present study indicated that miR-524-5p may function as a novel tumor suppressor gene in gastric cancer, and may serve as a biomarker and therapeutic target for the treatment of gastric cancer.

Entities:  

Keywords:  apoptosis; gastric cancer; invasion; miR-524-5p; proliferation

Year:  2016        PMID: 26998102      PMCID: PMC4774556          DOI: 10.3892/ol.2016.4143

Source DB:  PubMed          Journal:  Oncol Lett        ISSN: 1792-1074            Impact factor:   2.967


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