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. 2016 Jan 24;7(8):9069–9083. doi: 10.18632/oncotarget.6997

Figure 3. Ectopic expression of MYB is sufficient to overcome CDK9 inhibitor mediated apoptosis of ER+ve breast cancer cells.

Figure 3

A. AT7519 treatment has no effect on MYB levels in ectopic MYB-expressing MCF-7 cells. MCF-7-Myb and vector control MCF-7-Cont cell lines were incubated with AT7519 at the indicated concentrations for 4h and harvested to measure the expression of MYB by qPCR, with Cyclophilin A (PPIA) as an internal control. B. Ectopically-expressed MYB promotes survival of MCF-7 cells in the presence of Flavopiridol. MCF-7-Cont and (MCF-7-Myb) cells were incubated with Flavopiridol for 72h before performing Resazurin viability assays. Experiments were carried out twice in triplicate C. Ectopic MYB expression promotes resistance to apoptosis induced by CDK9i. MCF-7-Myb and -Control cell lines were incubated with either AT7519 (left panel) or Flavopiridol (right panel) for 60h before harvesting for AnnexinV/PI staining and FACS analysis. D. Fluorescence micrographs of cells from C. taken prior to harvesting. (E and F) AT7519 downregulates BCL-2 expression. MCF-7-Cont. and MCF-7-Myb cell lines were incubated for 4h or 16h with indicated dosages of AT7519 to determine the BCL-2 gene E. or protein expression F., respectively with β-actin gene and protein expression as internal and protein loading controls.