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. 2011 Aug 16;39(21):9194–9205. doi: 10.1093/nar/gkr658

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© The Author(s) 2011. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — Disruption of PCNA and DMAP1-binding domains of DNMT1 induces E-cadherin gene repression at the transcriptional level in the absence of changes in SNAIL1 expression. (A) Semiquantitative analysis of mRNA expression by RT–PCR of the indicated genes in HCT116 DNMT1^+/⁺, DNMT1^ΔE3⁻⁶ and DNMT3b⁻^/⁻ cells. A significant and repetitive reduction of E-cadherin mRNA is observed in DNMT1^ΔE3⁻⁶ cells. No differences are observed in total levels of SNAIL mRNA. Results shown are representative of at least three independent experiments. (B) Quantitative analysis of E-cadherin mRNA expression by qRT–PCR in HCT116 DNMT1^+/⁺, DNMT1^ΔE3⁻⁶ and DNMT3b⁻^/⁻ cells. Relative expression levels are normalized to actin expression. Results are representative of those from three experiments. (C) Normalized Luciferase/Renilla activities of reporter vectors transiently transfected in HCT116 DNMT1^+/⁺, DNMT1^ΔE3⁻⁶ and DNMT3b⁻^/⁻, containing either the human E-cadherin promoter (upper panel) or the human SNAIL11 promoter (lower panel). Reduced E-cadherin promoter activity is observed in DNMT1^ΔE3⁻⁶ cells, while no changes are observed in the activity of the SNAIL1 promoter. Analyses were performed in triplicate and the mean ± SD are shown. **P < 0.001.