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Abstract
Epigenetic parameters linked to E-cadherin gene were investigated in 5 human colorectal cancer cell lines. Treatment with trichostatin A led to enhanced acetylation of histone H3-K9 with concurrent induction of E-cadherin mRNA in 3 E-cadherin low/negative cell lines that are not DNA methylated. Co-treatment with 5-aza-2′-deoxycytidine and trichostatin A resulted in additive/synergic induction of E-cadherin mRNA in all 5 cell lines with concomitant enhancement of histone H3-K9 acetylation in 4 E-cadherin low/negative cell lines. Our results suggest that histone H3-K9 deacetylation appears to play a crucial role in transcriptional repression of E-cadherin in colorectal cancers.
| ABBREVIATIONS | ||
| E-cad | = | E-cadherin |
| CDH1 | = | E-cadherin gene |
| CRC | = | colorectal cancer |
| H3-K9 acetylation | = | acetylation of histone H3 (Lys 9) |
| H3-K9 methylation | = | methylation of histone H3 (Lys 9) |
| PMR | = | percentage of methylated reference |
| DAC | = | 5-aza-2′-deoxycytidine |
| TSA | = | trichostatin A |
| ABBREVIATIONS | ||
| E-cad | = | E-cadherin |
| CDH1 | = | E-cadherin gene |
| CRC | = | colorectal cancer |
| H3-K9 acetylation | = | acetylation of histone H3 (Lys 9) |
| H3-K9 methylation | = | methylation of histone H3 (Lys 9) |
| PMR | = | percentage of methylated reference |
| DAC | = | 5-aza-2′-deoxycytidine |
| TSA | = | trichostatin A |