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. 2019 Sep 5;10(4):615–627. doi: 10.1016/j.apsb.2019.08.008

Figure 1.

Figure 1

Synthetic lethality between HDAC inhibition and BRCA1 deficiency. (A) The effect of HDAC inhibitors on colony formation of T47D BRCA1 wildtype (shCTRL) and BRCA1 knock-down (shBRCA1) cell lines was tested. Cells were treated with the compounds for 15 days and cell colonies were stained with crystal violet reagent. (B)–(D) The effect of HDAC inhibitors on the cell viability of HCC1937 BRCA1 isogenic cell lines was tested. Cells were treated with the compounds for 3 days and cell viability was determined by alamarblue assay. (E) and (F) Flow cytometry was performed to analyze sub-G1 cell population (E) and annexin V-FITC staining (F) of HCC1937 BRCA1 isogenic cell lines after treated with 5 μmol/L entinostat for 72 h. (G) The effect of HDAC inhibitors on the nuclear morphology of HCC1937 BRCA1 isogenic cell lines was tested. Cells were treated with 5 μmol/L entinostat, vorinostat or mocetinostat for 72 h. Cell nuclei were stained with hoechst33342 reagent and observed under a fluorescent microscope. Scale bar = 100 μm. (H) Western blot analysis for PARP1 and cleaved caspase-3 in HCC1937 BRCA1 isogenic cells treated with 5 μmol/L entinostat for 72 h. Data are mean ± SD, **P < 0.01 between two groups.