Abstract: Objective To explore the effects of microRNA-125b (miR-125b) on the retinoblastoma multidrug resistance and to study its molecular mechanism of miR-125b on chemotherapy sensitivity. Design Experimental study. Participants The retinablastoma cell lines SO-RB50. Methods The expression of miR-125b was detected by real-time PCR in SO-RB50 cell line and SO-RB50/VCR cell line. The synthesized miR-125b mimic (miR-125mimic group) and miR-125b inhibitor (miR-125inhibitor group) was transfected into retinoblastoma SO-RB50 cell line. In addition, three chemotherapeutic drugs, including carboplatin, etoposide and vincristine, were used to treat the transfected SO-RB50 cell line respectively, in order to evaluate the sensitivity of RB cells. The cell proliferation and apoptosis were measured by MTT and Annexin V-FITC. The protein expression level of MGEA-A and P53 was detected in the transfected SO-RB50 cell line by Western blot. Main Outcome Measures The percentage of cell survival and the percentage of apoptotic cells to total cells. Results MiR-125b was significantly up-regulated （P=0.000）in the SO-RB50/VCR cell line compared to that in the SO-RB50 cell line (P=0.000). It apparently promotes RB cell proliferation and suppresses cell apoptosis（P=0.000） in the miR-125mimic group compared with that in the miR-125inhibitor group treated by carboplatin, etoposide and vincristine respectively （P=0.000）. The protein expression level of MAGE-A was higher significantly in the miR-125mimic group than in the miR-125inhibitor group（P=0.004）. Meanwhile, the protein expression level of P53 was lower significantly in the miR-125mimic group than in the miR-125inhibitor group (P=0.001). Conclusion The SO-RB50 cell line inhibited the expression of miR-125b was sensitive to carboplatin, etoposide and vincristine, and furthermore miR-125b/MAGE-A/p53 axis may be conducive to enhancing the efficacies of chemotherapeutic treatments for RB.

Key words: retinoblastoma, microRNA-125b, MAGE-A/P53, multidrug resistance