Histone deacetylase (HDAC) inhibitors, such as suberoylanilide hydroxamic acid (SAHA), selectively induce p21(WAF1) expression and gene-associated histone acetylation. SAHA, a hydroxamic acid-based compound, inhibits HDAC activity, leading to increased acetylation of histones H3 and H4 in the chromatin of the p21(WAF1) gene. This acetylation is associated with increased p21(WAF1) mRNA and protein expression in T24 bladder carcinoma cells. SAHA induces a 9-fold increase in p21(WAF1) mRNA and protein, which is at least partially due to increased transcription of the gene. SAHA causes an accumulation of acetylated histones H3 and H4 in total cellular chromatin by 2 hours, which is maintained through 24 hours of culture. The level of histone acetylation increases throughout the p21(WAF1) promoter and structural gene after SAHA treatment. However, no change in acetylation is observed in chromatin associated with the actin and p27 genes, and their mRNA expression is not altered. These findings suggest that SAHA-induced p21(WAF1) expression is regulated, at least in part, by the degree of acetylation of the gene-associated histones. SAHA-induced histone acetylation is gene-selective, as it does not affect the expression of the actin or p27 genes or the acetylation levels in their chromatin. The study also shows that SAHA inhibits the proliferation of T24 cells and induces a marked decrease in the proportion of cells in the S phase of the cell cycle. SAHA-induced p21(WAF1) expression is associated with a transient increase in acetylated histones in the chromatin of the p21(WAF1) gene. The transcription rate of the p21(WAF1) gene increases initially but decreases by 24 hours. The study concludes that SAHA selectively induces p21(WAF1) expression and gene-associated histone acetylation, which is associated with growth arrest in T24 cells. The mechanism of gene selectivity of SAHA-induced histone acetylation is not fully understood, but the findings suggest that SAHA is a potent inhibitor of tumor cell growth and is currently in Phase I clinical trials as a potential anticancer therapy.Histone deacetylase (HDAC) inhibitors, such as suberoylanilide hydroxamic acid (SAHA), selectively induce p21(WAF1) expression and gene-associated histone acetylation. SAHA, a hydroxamic acid-based compound, inhibits HDAC activity, leading to increased acetylation of histones H3 and H4 in the chromatin of the p21(WAF1) gene. This acetylation is associated with increased p21(WAF1) mRNA and protein expression in T24 bladder carcinoma cells. SAHA induces a 9-fold increase in p21(WAF1) mRNA and protein, which is at least partially due to increased transcription of the gene. SAHA causes an accumulation of acetylated histones H3 and H4 in total cellular chromatin by 2 hours, which is maintained through 24 hours of culture. The level of histone acetylation increases throughout the p21(WAF1) promoter and structural gene after SAHA treatment. However, no change in acetylation is observed in chromatin associated with the actin and p27 genes, and their mRNA expression is not altered. These findings suggest that SAHA-induced p21(WAF1) expression is regulated, at least in part, by the degree of acetylation of the gene-associated histones. SAHA-induced histone acetylation is gene-selective, as it does not affect the expression of the actin or p27 genes or the acetylation levels in their chromatin. The study also shows that SAHA inhibits the proliferation of T24 cells and induces a marked decrease in the proportion of cells in the S phase of the cell cycle. SAHA-induced p21(WAF1) expression is associated with a transient increase in acetylated histones in the chromatin of the p21(WAF1) gene. The transcription rate of the p21(WAF1) gene increases initially but decreases by 24 hours. The study concludes that SAHA selectively induces p21(WAF1) expression and gene-associated histone acetylation, which is associated with growth arrest in T24 cells. The mechanism of gene selectivity of SAHA-induced histone acetylation is not fully understood, but the findings suggest that SAHA is a potent inhibitor of tumor cell growth and is currently in Phase I clinical trials as a potential anticancer therapy.