Fig. 3: miR-30c potentiated the antitumor effect of ADR in vitro and in vivo.

a Real-time PCR analysis of miR-30c basal expression in wtp53 (MCF-10A, MCF-7, and ZR-75-1) and mutp53 (MDA-MB-231, and T-47D) BrCa cells. *p < 0.05, wtp53 vs. mutp53 BrCa. b wtp53 and mutp53 BrCa cells were treated with ADR (0.5 µM) for 48 h. The expression of miR-30c was evaluated by qRT-PCR. *p < 0.05,**p < 0.01 vs. control group. NS indicates no significant difference. c MDA-MB-231 and T47D cells were transiently transfected with the NC or miR-30c mimic and were treated with various ADR concentrations. The relative viability of the MDA-MB-231 and T47D cells was determined via CCK-8 assays (n = 3). *p < 0.05 vs. NC group. d The relative viability of the MDA-MB-231and T47D cells was detected by CCK-8 assays 48 h after transfection with NC (20 nM), miR-30c mimic (20 nM), FANCF (4 µg), REV1 cDNA(4 µg) or FANCF and REV1 cDNA. FANCF and REV1 constructs are plasmids without 3′ UTR region. ^#p < 0.05 vs. miR-30c group, *p < 0.05 vs. NC group. e MCF-7 and MDA-MB-231 cells were injected subcutaneously into nude mice. A cholesterol-conjugated miR-30c agomir or negative control (NC) agomir was intratumorally injected 7 days after tumor formation, and agomir and ADR were intratumorally injected every two days (n = 5). f Xenograft tumor growth was monitored. ^#p < 0.05, ^##p < 0.01 vs. ADR group; *p < 0.05, **p < 0.01 vs. NC(-) agomir group. g Tumor weight at sacrifice. *p < 0.05, ***p < 0.001 vs. NC(−) agomir group; ^#p < 0.05, ^###p < 0.001 vs. ADR group. Data represent the mean ± SD (n = 5, each group). h Photographs of the removed tumors at day 34 after the implantation. i Western blot analysis for FANCF and REV1 in the MCF-7 and MDA-MB-231 xenografts after treatment with the cholesterol-conjugated miR-30c agomir or the NC agomir. **p < 0.01 vs. NC group