Journal: Clinical Epigenetics

Article Title: HDAC8 suppresses the epithelial phenotype and promotes EMT in chemotherapy-treated basal-like breast cancer

doi: 10.1186/s13148-022-01228-4

Figure Lengend Snippet: 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

Article Snippet: Three cycles of 48-h treatment with PCI34051 (HDAC8 inhibitor, Cayman chemical, cat. no 10444) or TMP 195 (HDAC4 and HDAC7 inhibitor, Cayman chemical, cat. no 23242) were performed.

Techniques: Clone Assay, Quantitative RT-PCR, Proliferation Assay, Staining, Inhibition, Expressing

Journal: Clinical Epigenetics

Article Title: HDAC8 suppresses the epithelial phenotype and promotes EMT in chemotherapy-treated basal-like breast cancer

doi: 10.1186/s13148-022-01228-4

Figure Lengend Snippet: HDAC8 silencing or inhibition sensitizes BLBC cells to chemotherapy treatment. A ROC analysis from publically available TNBC data demonstrating that patients with poor response to chemotherapy harbor high expression levels of HDAC8. Box plots: Mann–Whitney test. B, C Proliferation assay of CAF-treated pG-2 ( B ) and rG-2 ( C ) cells upon Hdac8 silencing. Representative crystal violet pictures are at the right panel of the bar charts. D Proliferation assay of pG-2 treated with low CAF doses (156.25 ng/ml cyclophosphamide, 7.8 ng/ml doxorubicin, 156.25 ng/ml 5-FU) for 48 h, w/ or w/o HDAC8 inhibition (5 μM PCI34051). E rG-2 cells treated with CAF for 48 h, w/ or w/o HDAC8 (5 μM PCI34051). Representative crystal violet pictures are at the left and right panel of proliferation kinetic graphs for pG-2 and rG-2, respectively. F Proliferation assay of HCC1806 treated with low CAF doses (156.25 ng/ml cyclophosphamide, 7.8 ng/ml doxorubicin, 156.25 ng/ml 5-FU) for 48 h, w/ or w/o HDAC8 inhibition (10 μM PCI34051). All experiments were performed in biological triplicates. ns = no difference, * p -val < 0.05, *** p -val < 0.005, **** p -val < 0.001. Statistical test: Student's t test. Error bars are standard error of the mean (SEM)

Article Snippet: Three cycles of 48-h treatment with PCI34051 (HDAC8 inhibitor, Cayman chemical, cat. no 10444) or TMP 195 (HDAC4 and HDAC7 inhibitor, Cayman chemical, cat. no 23242) were performed.

Techniques: Inhibition, Expressing, MANN-WHITNEY, Proliferation Assay