Skip to main content
. Author manuscript; available in PMC: 2020 Jan 1.
Published in final edited form as: Mol Cancer Res. 2018 Sep 13;17(1):30–41. doi: 10.1158/1541-7786.MCR-18-0246

Figure 1. Restoration of miR-200c to TNBC represses epithelial to mesenchymal transition and pathways/genes involved in immune suppressive functions.

Figure 1.

BT549-TripZ-200c cells containing the pre-miR-200c sequence in the DOX inducible pTripZ vector were treated in triplicate with 1 μg/mL Doxycycline (DOX) or vehicle for 48 hours. (A) Heat map of differentially expressed genes (adjusted p-value < 0.10 and fold-change > 1.2) between untreated (DOX-) and induced (DOX+) BT549-TripZ-200c cells in triplicate. (B) In both BT549-TripZ-200c and BT549 cells with empty pTripZ vector (BT549-TripZ EV), miR-200c and ZEB1 were measured by qRT-PCR and normalized to U6 and 18S respectively, and presented as fold change of DOX+ cells relative to untreated counterpart cells. ****P<0.0001, unpaired t-test. (C) Western blot for ZEB-1 and E-Cadherin proteins in BT549-TripZ-EV cells and BT549-TripZ-200c minus or plus DOX (48 hrs). (D) Gene Set Enrichment Analysis of pathways enriched in DOX- (no miR-200c) versus DOX+ (miR-200c induced). **P<0.01, *P<0.05, unpaired t-test. (E) Select transcripts measured by qRT-PCR from RNA isolated from independent BT549–200c cells DOX- and DOX+ for 48 hours.