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Detection of promoter hypermethylation of the CpG island of E-cadherin in gastric cardiac adenocarcinoma

AIM: Abnormal hypermethylation of CpG islands associated with tumor suppressor genes can lead to transcriptional silencing in neoplasia. The aim of this study was to investigate the promoter methylation and expression of E-cadherin gene in gastric cardiac adenocarcinoma (GCA). METHODS: A nested MSP...

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Autores principales: Guo, W, Dong, Z, Guo, Y, Kuang, G, Yang, Z, Chen, Z
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352230/
https://www.ncbi.nlm.nih.gov/pubmed/19748854
http://dx.doi.org/10.1186/2047-783X-14-10-453
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author Guo, W
Dong, Z
Guo, Y
Kuang, G
Yang, Z
Chen, Z
author_facet Guo, W
Dong, Z
Guo, Y
Kuang, G
Yang, Z
Chen, Z
author_sort Guo, W
collection PubMed
description AIM: Abnormal hypermethylation of CpG islands associated with tumor suppressor genes can lead to transcriptional silencing in neoplasia. The aim of this study was to investigate the promoter methylation and expression of E-cadherin gene in gastric cardiac adenocarcinoma (GCA). METHODS: A nested MSP approach, immunohistochemistry method and RT-PCR were used respectively to examine the methylation status of the 5' CpG island of E-cadherin, its protein expression and mRNA expression in tumors and corresponding normal tissues. RESULTS: E-cadherin was methylated in 63 of 92 (68.5%) tumor specimens, which was significantly higher than that in corresponding normal tissues (P < 0.001). Methylation frequencies of stage III and IV tumor tissues was significantly higher than that in stage I and II tumor tissues (P = 0.01). Methylation status of poor differentiation group was significantly higher than moderate and poor-moderate differentiation groups (P < 0.01). By immunostaining 51 of 92 tumor tisssues demonstrated heterogeneous, positive immunostaining of tumor tissues (44.6%), significantly different from matched normal tissues (P < 0.001). Positive immunostaining of stage III and IV tumor tissues was significantly lower than stage I and II tumor tissues (P < 0.01). Poor differentiation group was also significantly lower than moderate and poor-moderate differentiation groups (P < 0.05). 80 percent of tumor tissues with E-cadherin gene methylated showed inactivated mRNA expression. CONCLUSIONS: High methylation status of the 5' CpG island of E-cadherin gene may be one of the mechanisms in the development of gastric cardiac adenocarcinoma.
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spelling pubmed-33522302012-05-16 Detection of promoter hypermethylation of the CpG island of E-cadherin in gastric cardiac adenocarcinoma Guo, W Dong, Z Guo, Y Kuang, G Yang, Z Chen, Z Eur J Med Res Research AIM: Abnormal hypermethylation of CpG islands associated with tumor suppressor genes can lead to transcriptional silencing in neoplasia. The aim of this study was to investigate the promoter methylation and expression of E-cadherin gene in gastric cardiac adenocarcinoma (GCA). METHODS: A nested MSP approach, immunohistochemistry method and RT-PCR were used respectively to examine the methylation status of the 5' CpG island of E-cadherin, its protein expression and mRNA expression in tumors and corresponding normal tissues. RESULTS: E-cadherin was methylated in 63 of 92 (68.5%) tumor specimens, which was significantly higher than that in corresponding normal tissues (P < 0.001). Methylation frequencies of stage III and IV tumor tissues was significantly higher than that in stage I and II tumor tissues (P = 0.01). Methylation status of poor differentiation group was significantly higher than moderate and poor-moderate differentiation groups (P < 0.01). By immunostaining 51 of 92 tumor tisssues demonstrated heterogeneous, positive immunostaining of tumor tissues (44.6%), significantly different from matched normal tissues (P < 0.001). Positive immunostaining of stage III and IV tumor tissues was significantly lower than stage I and II tumor tissues (P < 0.01). Poor differentiation group was also significantly lower than moderate and poor-moderate differentiation groups (P < 0.05). 80 percent of tumor tissues with E-cadherin gene methylated showed inactivated mRNA expression. CONCLUSIONS: High methylation status of the 5' CpG island of E-cadherin gene may be one of the mechanisms in the development of gastric cardiac adenocarcinoma. BioMed Central 2009-09-28 /pmc/articles/PMC3352230/ /pubmed/19748854 http://dx.doi.org/10.1186/2047-783X-14-10-453 Text en Copyright ©2009 I. Holzapfel Publishers
spellingShingle Research
Guo, W
Dong, Z
Guo, Y
Kuang, G
Yang, Z
Chen, Z
Detection of promoter hypermethylation of the CpG island of E-cadherin in gastric cardiac adenocarcinoma
title Detection of promoter hypermethylation of the CpG island of E-cadherin in gastric cardiac adenocarcinoma
title_full Detection of promoter hypermethylation of the CpG island of E-cadherin in gastric cardiac adenocarcinoma
title_fullStr Detection of promoter hypermethylation of the CpG island of E-cadherin in gastric cardiac adenocarcinoma
title_full_unstemmed Detection of promoter hypermethylation of the CpG island of E-cadherin in gastric cardiac adenocarcinoma
title_short Detection of promoter hypermethylation of the CpG island of E-cadherin in gastric cardiac adenocarcinoma
title_sort detection of promoter hypermethylation of the cpg island of e-cadherin in gastric cardiac adenocarcinoma
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352230/
https://www.ncbi.nlm.nih.gov/pubmed/19748854
http://dx.doi.org/10.1186/2047-783X-14-10-453
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