Skip to main content
Fig. 9 | Clinical Epigenetics

Fig. 9

From: Combined inhibition of histone deacetylase and cytidine deaminase improves epigenetic potency of decitabine in colorectal adenocarcinomas

Fig. 9

The effects of decitabine/PBA and THU on cell proliferation in CDA silenced colon cancer cell lines. A1 Treatment scheme. We treated Caco-2, HCT-116-p53wt and HCT-116-p53null cells with the single-stranded antisense oligonucleotides (ASO) for 24 h followed by the combined decitabine/PBA drug treatment for 5 days. A2 The effects of CDA gene knockdown on cell proliferation of colon cancer cell lines. Shown are the relative OD value of Caco-2, HCT-116-p53wt and HCT-116-p53null cells following single CDA gene knockdown. Gene silencing of CDA inhibited cell viability when compared with vector controls. Statistical analysis: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. A3 Inhibition of cell proliferation in CDA silenced colon cancer cell lines following combined decitabine/PBA treatment. CDA gene knockdown improved therapeutic efficacy of the combined decitabine/PBA treatment significantly and caused 70–95% inhibition of cell viability among the three colon cancer cell lines. Statistical analysis: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. A4 DNA synthesis in CDA silenced colon cancer cell lines. CDA gene knockdown of colon cancer cell lines inhibited DNA synthesis as determined by the BrdU labeling assay. Depending on the cell line, the inhibition of DNA synthesis ranged between 20% (HCT-116-p53null) to 70% (HCT-116-p53wt). Additional decitabine/PBA treatment was most effective in inhibiting DNA synthesis (range 80–90%). Statistical analysis: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. B1 Inhibition of cell proliferation of colon cancer cell lines following daily THU treatment at different drug concentration for 48 h. We treated Caco-2, HCT-116-p53wt and HCT-116-p53null cells with various drug concentrations of the CDA inhibitor THU. At 80 µg/ml THU the inhibition of cell proliferation ranged between 35 and 48%. Statistical analysis: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. B2 Effects of various THU drug concentrations on DNA synthesis in colon cancer cell lines. We treated Caco-2, HCT-116-p53wt and HCT-116-p53null cells with varying concentrations of the CDA inhibitor THU. At 80 µg/ml THU the inhibition of DNA synthesis ranged between 30 and 40%. The combined THU /decitabine treatment of colon cancer cells was more effective in inhibiting DNA synthesis (range 40–60%). Statistical analysis: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001

Back to article page