Additional file 5: Figure S5. of Overexpression of the miR-141/200c cluster promotes the migratory and invasive ability of triple-negative breast cancer cells through the activation of the FAK and PI3K/AKT signaling pathways by secreting VEGF-A

microRNA expression levels of miR-200 cluster transduced MCF-7, MDA-MB-231, HCC-38, and Hs578T cells. Quantitative real-time RT-PCR of microRNAs (miR-200a, miR-200b, and miR-200c). (A, B, C) microRNAs in MCF-7 cells. The miR-200ab cells transduced with the miR-200b/200a/429 cluster exhibited high levels of expression of miR-200a (~60-fold) and miR-200b (~40-fold) relative to those of the control cells. The miR-200c cells transduced with the miR-200c/141 cluster exhibited remarkably high levels of expression of miR-200c (~266-fold) relative to those of the control cells. (D, E, F) microRNAs in MDA-MB-231. The miR-200ab cells transduced with the miR-200b/200a/429 cluster exhibited high expression levels of miR-200a (~6-fold) and miR-200b (~40-fold) relative to those of the control cells. The miR-200c cells transduced with the miR-200c/141 cluster exhibited remarkably high expression levels of miR-200c (~93-fold) relative to those of the control cells. (G) microRNAs in HCC-38. The miR-200c cells transduced with the miR-200c/141 cluster exhibited remarkably high expression levels of miR-200c (~252-fold) relative to those of the control cells. (H) microRNAs in Hs578T. The miR-200c cells transduced with the miR-200c/141 cluster exhibited remarkably high expression levels of miR-200c (~205-fold) relative to those of the control cells. *p < 0.05, **p < 0.001. (JPG 50 kb)