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. Author manuscript; available in PMC: 2017 Sep 28.
Published in final edited form as: Sci Signal. 2016 Dec 6;9(457):ra118. doi: 10.1126/scisignal.aaf5402

Figure 7. TGFβ inhibition of miR-182 mediates BRCA1 and mammary phenotype.

Figure 7

(A-C) MCF10A cell lines engineered to stably express mirZip-182 or miRZip-SCR were compared using qRT-PCR to measure (A) miR-182(B) BRCA1 and (C) FOXO3 mRNA. The abundance of each in MCF10 cells expressing miRZip-182 was normalized to that in cells expressing miRZip-SCR. Data are means ±S.E.M. of 4 or more independent experiments analyzed using Student's t-test. (D and E) qRT-PCR (D) BRCA1 or (E) FOXO3 mRNA abundance measured in MCF10A cell lines engineered to stably express miRZip-SCR (left) or mirZip-182 (right) in response to TGFβ and/or LY364947 normalized to their respective untreated controls. Data are means ± S.E.M from 4 independent experiments, analyzed using ANOVA. (F) Abundance of miR-182 in Tgfb1 HT MEC infected with miRZIP-182 lentivirus compared to HT MEC and WT MEC transfected with miR-ZIP SCR. (G) Quantitation of immunoblots for BRCA1 and FOXO3 in (F). (H) Mammosphere forming efficiency of HT and WT MEC expressing miRZip-182 or mirZip-SCR. Data are means ± S.D. from 2 biological replicates. (I) Mammospheres from (H) analyzed for percentage of cells staining positively for the basal/myoepithelial marker p63. Data are means ± S.D. from 17 mammospheres, pooled from two independent experiments; *P<0.05, **P<0.01, ***P<0.001, by Student's t-test.