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Transcriptional repression of the transforming growth factor-β type I receptor gene by DNA methylation results in the development of TGF-β resistance in human gastric cancer

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dc.contributor.authorKang, Shin Hyeok-
dc.contributor.authorBang, Yung-Jue-
dc.contributor.authorIm, Young-Hyuck-
dc.contributor.authorYang, Han-Kwang-
dc.contributor.authorLee, David A-
dc.contributor.authorLee, Hwa Young-
dc.contributor.authorLee, Ho Soon-
dc.contributor.authorKim, Noe Kyeong-
dc.contributor.authorKim, Seong-Jin-
dc.date.accessioned2021-01-31T11:59:56Z-
dc.date.available2021-01-31T11:59:56Z-
dc.date.issued1999-12-
dc.identifier.citationOncogene, Vol.18 No.51, pp.7280-7286-
dc.identifier.issn0950-9232-
dc.identifier.other119595-
dc.identifier.urihttps://hdl.handle.net/10371/173195-
dc.description.abstractThe transforming growth factor-beta (TGF-beta) signaling pathway subserves an essential tumor suppressor function in various cell types. A heteromeric complex composed of TGF-beta type I (RI) and type II (RII) receptors is required for TGF-beta signaling. We have identified a subset of human gastric cancer cell lines which are insensitive to TGF-beta and which express a low level of TGF-beta type I receptor mRNA relative to a gastric cancer cell line which is highly responsive to TGF-beta. Using these cells, we show that hypermethylation of a CpG island in the 5' region of the TGF-beta RI gene provides another potentially important mechanism of escape from negative growth control by TGF-beta, This hypermethylation was found in four of five human gastric cancer cell lines and five out of 40 (12.5%) primary tumors examined, In human gastric cancer cell lines, treatment with the demethylating agent, 5-aza-2'-deoxycytidine, resulted in increased expression of the TGF-beta RI gene, but not the RII gene, Transient transfection of an RI expression vector into the TGF-beta resistant SNU-601 cell line restores TGF-beta responsiveness. These findings suggest that one of the mechanisms of escape from autocrine or paracrine growth control by TGF-beta during carcinogenesis could involve aberrant methylation of CpG islands in the 5' region of the TGF-beta RI gene.-
dc.subjecttransforming growth factor-beta-
dc.subjectCpG methylation-
dc.subjectcancer-
dc.subjectreceptor-
dc.titleTranscriptional repression of the transforming growth factor-β type I receptor gene by DNA methylation results in the development of TGF-β resistance in human gastric cancer-
dc.typeArticle-
dc.contributor.AlternativeAuthor방영주-
dc.identifier.doi10.1038/sj.onc.1203146-
dc.citation.journaltitleOncogene-
dc.identifier.scopusid2-s2.0-0000031048-
dc.citation.endpage7286-
dc.citation.number51-
dc.citation.startpage7280-
dc.citation.volume18-
dc.identifier.urlhttps://www.nature.com/articles/1203146-
dc.identifier.rimsid119595-
dc.identifier.sci000084119400012-
dc.contributor.affiliatedAuthorBang, Yung-Jue-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Internal Medicine (내과학전공)Journal Papers (저널논문_내과학전공)
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