Fig. 2

HDAC4, HDAC7 and HDAC8 are upregulated in CAF-treated pG-2 and in CAF-resistant clones. A Heatmap of differentially regulated epigenetic factors in pG-2 cells upon CAF treatment (48 h) (basemean ≥ 15, p-adj < 0.05, log2FC ≥|0.7|). B qRT-PCR of Hdac4, Hdac7, Hdac8 in vehicle- and CAF-treated (48 h) pG-2 cells. C, D qRT-PCR validating the efficiency of HDAC4, HDAC7 and HDAC8 knockdowns in pG-2 (C) and HCC1806 (D), respectively. E Proliferation assay of pG-2 and HCC1806 cells upon HDAC4, HDAC7 and HDAC8 silencing, assessed by crystal violet staining. F Proliferation assay of pG-2 and HCC1806 cells upon HDAC8 inhibition (5 μM and 20 μM PCI34051, respectively) or HDAC4/HDAC7 inhibition (4 μM and 2 μM TMP195, respectively), assessed by crystal violet staining. G Kaplan–Meier plots showing the overall survival probability of HDAC4-, HDAC7- and HDAC8-expressing BLBC patients (expression and survival data are from the TCGA-BRCA database). All experiments were performed in triplicate. ns = not significant, *p-val < 0.05, ***p-val < 0.005. Statistical test: B Student's t test, error bars: standard error of the mean (SEM); G Log-rank test