Figure 1
Dose-dependent hypomethylation induction by DAC in different cell lines. (A) IC50 of DAC, AZA, and Ara-C in human cancer cell lines. We measured IC50 of DAC, AZA, and Ara-C in a panel of human cancer cell lines, and correlated IC50 of DAC versus IC50 of Ara-C, IC50 of DAC versus IC50 of AZA, respectively. (B) Dose-dependent hypomethylation induction by DAC in different cell lines. After treatment with DAC for 4 days, cells were collected, and DNA was extracted. LINE methylation was measured by bisulfite pyrosequencing analysis. In each cell line, except the most resistant cells (bottom graph), the dose-dependent curve was U-shaped. (B) Absence of correlation of the IC50 of DAC with LINE methylation at baseline (R = 0.05, P = .97). (C) Correlation between the IC50 of DAC with the doses of DAC required for the maximum hypomethylation of LINE (R = 0.94, P < .001).

Dose-dependent hypomethylation induction by DAC in different cell lines. (A) IC50 of DAC, AZA, and Ara-C in human cancer cell lines. We measured IC50 of DAC, AZA, and Ara-C in a panel of human cancer cell lines, and correlated IC50 of DAC versus IC50 of Ara-C, IC50 of DAC versus IC50 of AZA, respectively. (B) Dose-dependent hypomethylation induction by DAC in different cell lines. After treatment with DAC for 4 days, cells were collected, and DNA was extracted. LINE methylation was measured by bisulfite pyrosequencing analysis. In each cell line, except the most resistant cells (bottom graph), the dose-dependent curve was U-shaped. (B) Absence of correlation of the IC50 of DAC with LINE methylation at baseline (R = 0.05, P = .97). (C) Correlation between the IC50 of DAC with the doses of DAC required for the maximum hypomethylation of LINE (R = 0.94, P < .001).

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