Abstract
Objective To observe the effect and mechanism of microRNA (miRNA, miR)-26a on the proliferation of triple negative breast cancer cells. Methods The effect of miR-26a on cell proliferation was detected by methyl thiazol tetrazolium (MTT) assay and colony formation assay, the effect of miR-26a on cell cycle was detected by flow cytometry. Use miRTarBase to predict target genes of miR-26a. In hundreds of target genes, we screened oncogene c-Myc as the research object. Use Western blotting test to detect the expression of c-Myc and its downstream target genes Cyclin D2 and Cyclin E1 in triple negative breast cancer cell lines after miR-26a overexpression. Results MTT assay revealed that the proliferation activity of miR-26a mimic transfection group was significantly lower than that of miR-mimic NC transfection group. Colony formation assay revealed that the cell clone ability of miR-26a mimic transfection group was significantly lower than that of miR-mimic NC transfection group [(55.67±5.86) cells vs. (144.33±5.03) cells; (62.00±3.00) cells vs. (107.67±2.52) cells, P<0.01]. Flow cytometry showed that the proportion of cells in G1 phase in the miRNA-26a mimic transfection group was significantly higher than that in the miRNA-mimic NC transfection group [(59.39±1.04)% vs. (46.91±1.04)%; (76.91±1.43)% vs. (63.21±1.61)%, P<0.01]. Western blotting test revealed that the expression of c-Myc and its downstream target genes Cyclin D2 and Cyclin E1 were significantly decreased. Conclusion MiR-26a may inhibit the proliferation of triple negative breast cancer by targeting the oncogene c-Myc. Key words: MicroRNA-26a; C-Myc; Triple negative breast cancer; Proliferation
Published Version
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