OBJECTIVE: To investigate the changes in cisplatin sensitivity of resistant ovarian cancer A2780 cells after inhibition of miR-23a expression and explore the molecular mechanisms. METHODS: The drug-resistant ovarian cancer A2780 cells were exposed to cisplatin alone or in combination with antagomir-23a. The cell inhibition rates after the treatments were detected using 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-23 a combined with cisplatin treatment significantly increased the cell inhibition rate (P<0.01) and lowered the IC(50) so of cisplatin by 83.76% 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 cellular expression of P-gp protein was significantly reduced as the cisplatin doses increased (P<0.01). CONCLUSION: Inhibition of miR-23a expression increases the sensitivity of A2780 cells to cisplatin possibly by inhibiting the negative regulation by miR-23a target genes that causes inhibition of P-gp protein expression.
OBJECTIVE: To investigate the changes in cisplatin sensitivity of resistant ovarian cancer A2780 cells after inhibition of miR-23a expression and explore the molecular mechanisms. METHODS: The drug-resistant ovarian cancer A2780 cells were exposed to cisplatin alone or in combination with antagomir-23a. The cell inhibition rates after the treatments were detected using 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-23 a combined with cisplatin treatment significantly increased the cell inhibition rate (P<0.01) and lowered the IC(50) so of cisplatin by 83.76% 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 cellular expression of P-gp protein was significantly reduced as the cisplatin doses increased (P<0.01). CONCLUSION: Inhibition of miR-23a expression increases the sensitivity of A2780 cells to cisplatin possibly by inhibiting the negative regulation by miR-23a target genes that causes inhibition of P-gp protein expression.