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Article: Epigenetic change in e-cardherin and COX-2 to predict chronic periodontitis

TitleEpigenetic change in e-cardherin and COX-2 to predict chronic periodontitis
Authors
Issue Date2010
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.translational-medicine.com/home/
Citation
Journal Of Translational Medicine, 2010, v. 8 How to Cite?
AbstractBackground: DNA methylation of certain genes frequently occurs in neoplastic cells. Although the cause remains unknown, many genes have been identified with such atypical methylation in neoplastic cells. The hypermethylation of E-Cadherin and Cyclooxygenase 2 (COX-2) in chronic inflammation such as chronic periodontitis may demonstrate mild lesion/mutation epigenetic level. This study compares the hypermethylation status of E-Cadherin and COX-2 genes which are often found in breast cancer patients with that in chronic periodontitis.Methods: Total DNA was extracted from the blood samples of 108 systemically healthy non-periodontitis subjects, and the gingival tissues and blood samples of 110 chronic periodontitis patient as well as neoplastic tissues of 106 breast cancer patients. Methylation-specific PCR for E-Cadherin and COX-2 was performed on these samples and the PCR products were analyzed on 2% agarose gel.Results: Hypermethylation of E-Cadherin and COX-2 was observed in 38% and 35% of the breast cancer samples, respectively. In chronic periodontitis patients the detection rate was 25% and 19% respectively, and none was found in the systemically healthy non-periodontitis control subjects. The hypermethylation status was shown to be correlated among the three groups with statistical significance (p < 0.0001). The methylation of CpG islands in E-Cadherin and COX-2 genes in periodontitis patients occurs more frequently in periodontitis patients than in the control subjects, but occurs less frequently than in the breast cancer patients.Conclusions: This set of data shows that the epigenetic change in E-Cadherin and Cyclooxygenase-2 is associated with chronic periodontitis. The epigenetic changes presented in chronic inflammation patients might demonstrate an irreversible destruction in the tissues or organs similar to the effects of cancer. Chronic periodontitis to some extent might be associated with DNA hypermethylation which is related to cancer risk factors. © 2010 Loo et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/137168
ISSN
2023 Impact Factor: 6.1
2023 SCImago Journal Rankings: 1.611
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Science and Technology Department of Sichuan province, China2007SGY028
Department of Sichuan province, China2007SGY028
Funding Information:

This study was supported by Scientific Support Project of Science and Technology Department of Sichuan province, China (2007SGY028).

References

 

DC FieldValueLanguage
dc.contributor.authorLoo, WTYen_HK
dc.contributor.authorJin, Len_HK
dc.contributor.authorCheung, MNBen_HK
dc.contributor.authorWang, Men_HK
dc.contributor.authorChow, LWCen_HK
dc.date.accessioned2011-08-26T14:13:48Z-
dc.date.available2011-08-26T14:13:48Z-
dc.date.issued2010en_HK
dc.identifier.citationJournal Of Translational Medicine, 2010, v. 8en_HK
dc.identifier.issn1479-5876en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137168-
dc.description.abstractBackground: DNA methylation of certain genes frequently occurs in neoplastic cells. Although the cause remains unknown, many genes have been identified with such atypical methylation in neoplastic cells. The hypermethylation of E-Cadherin and Cyclooxygenase 2 (COX-2) in chronic inflammation such as chronic periodontitis may demonstrate mild lesion/mutation epigenetic level. This study compares the hypermethylation status of E-Cadherin and COX-2 genes which are often found in breast cancer patients with that in chronic periodontitis.Methods: Total DNA was extracted from the blood samples of 108 systemically healthy non-periodontitis subjects, and the gingival tissues and blood samples of 110 chronic periodontitis patient as well as neoplastic tissues of 106 breast cancer patients. Methylation-specific PCR for E-Cadherin and COX-2 was performed on these samples and the PCR products were analyzed on 2% agarose gel.Results: Hypermethylation of E-Cadherin and COX-2 was observed in 38% and 35% of the breast cancer samples, respectively. In chronic periodontitis patients the detection rate was 25% and 19% respectively, and none was found in the systemically healthy non-periodontitis control subjects. The hypermethylation status was shown to be correlated among the three groups with statistical significance (p < 0.0001). The methylation of CpG islands in E-Cadherin and COX-2 genes in periodontitis patients occurs more frequently in periodontitis patients than in the control subjects, but occurs less frequently than in the breast cancer patients.Conclusions: This set of data shows that the epigenetic change in E-Cadherin and Cyclooxygenase-2 is associated with chronic periodontitis. The epigenetic changes presented in chronic inflammation patients might demonstrate an irreversible destruction in the tissues or organs similar to the effects of cancer. Chronic periodontitis to some extent might be associated with DNA hypermethylation which is related to cancer risk factors. © 2010 Loo et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_US
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.translational-medicine.com/home/en_HK
dc.relation.ispartofJournal of Translational Medicineen_HK
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.en_US
dc.subject.meshBreast Neoplasms - genetics-
dc.subject.meshCadherins - genetics-
dc.subject.meshChronic Periodontitis - diagnosis - genetics-
dc.subject.meshCyclooxygenase 2 - genetics-
dc.subject.meshEpigenesis, Genetic-
dc.titleEpigenetic change in e-cardherin and COX-2 to predict chronic periodontitisen_HK
dc.typeArticleen_HK
dc.identifier.emailJin, L:ljjin@hkucc.hku.hken_HK
dc.identifier.authorityJin, L=rp00028en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/1479-5876-8-110en_HK
dc.identifier.pmid21047437en_HK
dc.identifier.pmcidPMC2998472-
dc.identifier.scopuseid_2-s2.0-78049371701en_HK
dc.identifier.hkuros184389en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78049371701&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume8en_HK
dc.identifier.isiWOS:000285146700001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLoo, WTY=7003567474en_HK
dc.identifier.scopusauthoridJin, L=7403328850en_HK
dc.identifier.scopusauthoridCheung, MNB=7201897548en_HK
dc.identifier.scopusauthoridWang, M=36079147700en_HK
dc.identifier.scopusauthoridChow, LWC=34975216600en_HK
dc.identifier.citeulike8208192-
dc.identifier.issnl1479-5876-

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