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Article: An investigation of the potential for epigenetic inactivation by transcription read-through in a sporadic colorectal cancer

TitleAn investigation of the potential for epigenetic inactivation by transcription read-through in a sporadic colorectal cancer
Authors
KeywordsTranscription read-through
DNA methylation
Epigenetic inactivation
Issue Date2016
Citation
Gene, 2016, v. 585, n. 1, p. 154-158 How to Cite?
Abstract© 2016 Elsevier B.V. Aberrant transcription read-through of a gene promoter as a result of genetic structural rearrangements can cause the epigenetic inactivation of a neighbouring gene. All reported cases have involved copy number alterations that remove the 3' poly(A) transcription terminator sequence of a gene leading to transcription read-through (TRT) and methylation of the gene promoter of a downstream gene. We aimed to determine whether deletion of poly (A) transcription terminator sequences was associated with the methylation of neighbouring genes in a CRC with extensive copy number alterations. We performed a high resolution CGH array and methylation analysis on a CRC specimen to identify such alterations. Analysis of the CRC using high-resolution CGH identified 6 genes with deletions in the 3' part of the gene that encompassed the poly(A) transcription terminator sequence. Bisulphite sequencing of the promoter region of neighbouring (affected) genes at these six regions showed all candidate genes were unmethylated. Considering the fact that six TRT affected genes in a CRC with multiple deletions show no signs of hypermethylated promoters, it would be fairly appropriate to suggest that epigenetic inactivation by TRT might be a rare phenomenon in sporadic CRCs.
Persistent Identifierhttp://hdl.handle.net/10722/251152
ISSN
2023 Impact Factor: 2.6
2023 SCImago Journal Rankings: 0.725
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSrivastava, Sameer-
dc.contributor.authorLudwig, Anne K.-
dc.contributor.authorWong, Jason W.H.-
dc.contributor.authorHesson, Luke B.-
dc.date.accessioned2018-02-01T01:54:45Z-
dc.date.available2018-02-01T01:54:45Z-
dc.date.issued2016-
dc.identifier.citationGene, 2016, v. 585, n. 1, p. 154-158-
dc.identifier.issn0378-1119-
dc.identifier.urihttp://hdl.handle.net/10722/251152-
dc.description.abstract© 2016 Elsevier B.V. Aberrant transcription read-through of a gene promoter as a result of genetic structural rearrangements can cause the epigenetic inactivation of a neighbouring gene. All reported cases have involved copy number alterations that remove the 3' poly(A) transcription terminator sequence of a gene leading to transcription read-through (TRT) and methylation of the gene promoter of a downstream gene. We aimed to determine whether deletion of poly (A) transcription terminator sequences was associated with the methylation of neighbouring genes in a CRC with extensive copy number alterations. We performed a high resolution CGH array and methylation analysis on a CRC specimen to identify such alterations. Analysis of the CRC using high-resolution CGH identified 6 genes with deletions in the 3' part of the gene that encompassed the poly(A) transcription terminator sequence. Bisulphite sequencing of the promoter region of neighbouring (affected) genes at these six regions showed all candidate genes were unmethylated. Considering the fact that six TRT affected genes in a CRC with multiple deletions show no signs of hypermethylated promoters, it would be fairly appropriate to suggest that epigenetic inactivation by TRT might be a rare phenomenon in sporadic CRCs.-
dc.languageeng-
dc.relation.ispartofGene-
dc.subjectTranscription read-through-
dc.subjectDNA methylation-
dc.subjectEpigenetic inactivation-
dc.titleAn investigation of the potential for epigenetic inactivation by transcription read-through in a sporadic colorectal cancer-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.gene.2016.03.031-
dc.identifier.pmid27016300-
dc.identifier.scopuseid_2-s2.0-84963705013-
dc.identifier.volume585-
dc.identifier.issue1-
dc.identifier.spage154-
dc.identifier.epage158-
dc.identifier.eissn1879-0038-
dc.identifier.isiWOS:000375519400022-
dc.identifier.issnl0378-1119-

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