Fig. 6

MiR-106a contributed to increased ABCG2 expression and diminished doxorubicin sensitivity in TNBC. By real-time PCR analysis, human recombinant CXCL1 dose-dependently decreased miR-106a expression in MDA-MB-231 cells (a), and neutralizing CXCL1 by CXCL1 neutralizing antibody reversed the expression of miR-106a which was reduced by hAdSCs’ CM (b). IgG was used as negative control antibody. c Transfection of miR-106a inhibitor (5 or 50 nM) dose-dependently increased ABCG2 protein expression in MDA-MB-231 cells, and the effect of doxorubicin-induced cell death was antagonized by transfection of 50 nM miR-106a inhibitor but not negative control inhibitor (d). Graphs showed mean ± SD of three independent experiments. *p < 0.05; **p < 0.01; *p < 0.001 to control group. ^## p < 0.01 to hAdSC CM group in (B) or to negative control-transfected treated with doxorubicin group in (D). Ab CXCL1 neutralizing antibody, CM conditioned medium, con control, doxo doxorubicin, hAdSCs human adipose-derived stem cells, IgG isotype control antibody, inh miR-106a inhibitor, NC negative control inhibitor