Journal of Southern Medical University ›› 2015, Vol. 35 ›› Issue (01): 125-.
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Abstract: Objective To investigate the changes in cisplatin sensitivity of resistant ovarian cancer A2780 cells after inhibition ofmiR-23a expression and explore the molecular mechanisms. Methods The drug-resistant ovarian cancer A2780 cells wereexposed to cisplatin alone or in combination with antagomir-23a. The cell inhibition rates after the treatments were detectedusing MTT assay, cell cycle changes assessed with flow cytometry, and apoptotic cells observed using Hoechst33258 staining.The changes in glycoprotein P-gp expression in the cells were detected using Western blotting. Results Inhibition of miR-23acombined with cisplatin treatment significantly increased the cell inhibition rate (P<0.01) and lowered the IC50 of cisplatin by83.76% from 110.18 μmol/L in the control group to 17.89 μmol/L (P<0.01). The combined treatments also caused cell cycle arrestin G0/G1 phase, increased the cell apoptosis rate (P<0.01) and the number of cells stained with Hoechst33258; the cellularexpression of P-gp protein was significantly reduced as the cisplatin doses increased (P<0.01). Conclusion Inhibition ofmiR-23a expression increases the sensitivity of A2780 cells to cisplatin possibly by inhibiting the negative regulation bymiR-23a target genes that causes inhibition of P-gp protein expression.
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https://www.j-smu.com/EN/Y2015/V35/I01/125