Carcinogenesis, Teratogenesis & Mutagenesis ›› 2017, Vol. 29 ›› Issue (6): 454-459.doi: 10.3969/j.issn.1004-616x.2017.06.010

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Regulatory mechanism of miR-202 on proliferation of A549 lung cancer cells

PENG Hui, MA Shumei, HONG Weiwei, SUI Jing, ZHANG Yanqiu, LIANG Geyu   

  1. Key Laboratory of Environmental Medicine Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, Jiangsu, China
  • Received:2017-07-07 Revised:2017-11-12 Online:2017-11-30 Published:2017-11-30

Abstract: OBJECTIVE:To investigate the regulatory mechanism on proliferation of miR-202 in A549 lung cancer cells. METHODS:Through the lentivirus transfection into A549 cells,up-and down-expression of miR-202 were investigated. DIANA-TOOLs and KEGG database were used to analyze the bioinformatic of miR-202 expression and to explore the signaling pathways that might be involved with potential target genes. Then,MTT assay and flow cytometry technology were applied to detect the influence of miR-202 on cell proliferation,apoptosis and cycle. RT-qPCR and Western blot methods were applied to detect the miR-202 regulation for its predicted target gene on both mRNA and protein levels. RESULTS:Bioinformatics analysis show that,miR-202 was involved in non-small cell lung cancer and other tumor-related pathways,and possibly in regulation of PIK3CA. Functional studies show that,compared with the negative control group,up-regulation of miR-202 inhibited cell proliferation (P < 0.05),caused cell cycle G1/S phase arrest (P < 0.05),but did not affect cell apoptosis (P > 0.05). Target gene study show that,compared with the control group,up-regulation of miR-202 reduced the expression of PIK3CA protein (P < 0.05),but had no effect on the expression of PIK3CA mRNA(P > 0.05). CONCLUSION:Expression of miR-202 influenced the proliferation and cycle of A549 cells through the negative regulation of PIK3CA and the study provides a new clue to the role and mechanism of miRNA in lung cancer.

Key words: Lung cancer, miR-202, cell proliferation, cell cycle, regulatory mechanism

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