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Article: Identification and characterization of genes whose expressions are altered in rat 6 fibroblasts transformed by mutant p53(val135)

TitleIdentification and characterization of genes whose expressions are altered in rat 6 fibroblasts transformed by mutant p53(val135)
Authors
Issue Date1999
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical And Biophysical Research Communications, 1999, v. 266 n. 2, p. 472-480 How to Cite?
AbstractThe wild-type tumor suppressor gene p53 is known as a transcription factor in activating or suppressing target genes that encode proteins in regulating genome stability, DNA damage, cell arrest, and apoptosis. However, the role of mutant p53 in the process of cell transformation is still unclear. Our recent work indicated that overexpression of mutant p53(val135) induced high incidence of spontaneous transformation in prolonged cultures of Rat 6 fibroblasts. In order to identify genes related to neoplastic transformation induced by the mutant p53, the p53(val135)-overexpressor R6 13-8 and its derived spontaneously transformed cell line T2 were analyzed by mRNA differential display. In a systematic screening with 80 primer sets of RT-PCR reactions, three genes were found to be differentially expressed between R6 13-8 and T2 cells. Two genes, identified as homologues of the growth factor inducible immediate-early gene Cyr61 and the human nonmuscle myosin heavy chain-B, were down-regulated in T2 cells. Interestingly, both genes were also suppressed in Rat 6 cells transformed by c-H-ras and v-myc, but not by v-src genes. The third gene is a homologue of the frizzled related protein, a gene family that acts, in some cases, as an antagonist to the Wnt signaling pathway. It is intriguing that the rat homologue of the frizzled related protein was only expressed in p53(val135)-overexpressing cells, but not in the parental Rat 6 cells. However, the same gene was also highly expressed in ras-transformed Rat 6 cells, and moderately expressed in v-src-transformed Rat 6 cells. This is the first study in which the association of mutant p53 to these three genes is revealed. Our current report may provide new clues to the role of mutant p53 in the process of cell transformation.
Persistent Identifierhttp://hdl.handle.net/10722/148180
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYam, JWPen_US
dc.contributor.authorZheng, JYen_US
dc.contributor.authorHsiao, WLWen_US
dc.date.accessioned2012-05-29T06:11:17Z-
dc.date.available2012-05-29T06:11:17Z-
dc.date.issued1999en_US
dc.identifier.citationBiochemical And Biophysical Research Communications, 1999, v. 266 n. 2, p. 472-480en_US
dc.identifier.issn0006-291Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/148180-
dc.description.abstractThe wild-type tumor suppressor gene p53 is known as a transcription factor in activating or suppressing target genes that encode proteins in regulating genome stability, DNA damage, cell arrest, and apoptosis. However, the role of mutant p53 in the process of cell transformation is still unclear. Our recent work indicated that overexpression of mutant p53(val135) induced high incidence of spontaneous transformation in prolonged cultures of Rat 6 fibroblasts. In order to identify genes related to neoplastic transformation induced by the mutant p53, the p53(val135)-overexpressor R6 13-8 and its derived spontaneously transformed cell line T2 were analyzed by mRNA differential display. In a systematic screening with 80 primer sets of RT-PCR reactions, three genes were found to be differentially expressed between R6 13-8 and T2 cells. Two genes, identified as homologues of the growth factor inducible immediate-early gene Cyr61 and the human nonmuscle myosin heavy chain-B, were down-regulated in T2 cells. Interestingly, both genes were also suppressed in Rat 6 cells transformed by c-H-ras and v-myc, but not by v-src genes. The third gene is a homologue of the frizzled related protein, a gene family that acts, in some cases, as an antagonist to the Wnt signaling pathway. It is intriguing that the rat homologue of the frizzled related protein was only expressed in p53(val135)-overexpressing cells, but not in the parental Rat 6 cells. However, the same gene was also highly expressed in ras-transformed Rat 6 cells, and moderately expressed in v-src-transformed Rat 6 cells. This is the first study in which the association of mutant p53 to these three genes is revealed. Our current report may provide new clues to the role of mutant p53 in the process of cell transformation.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_US
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Transformation, Neoplastic - Geneticsen_US
dc.subject.meshCloning, Molecularen_US
dc.subject.meshGene Expression Regulation - Geneticsen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshMutationen_US
dc.subject.meshRna, Messenger - Geneticsen_US
dc.subject.meshRatsen_US
dc.subject.meshSequence Analysisen_US
dc.subject.meshTumor Suppressor Protein P53 - Geneticsen_US
dc.titleIdentification and characterization of genes whose expressions are altered in rat 6 fibroblasts transformed by mutant p53(val135)en_US
dc.typeArticleen_US
dc.identifier.emailYam, JWP:judyyam@pathology.hku.hken_US
dc.identifier.authorityYam, JWP=rp00468en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1006/bbrc.1999.1852en_US
dc.identifier.pmid10600527-
dc.identifier.scopuseid_2-s2.0-0033590213en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033590213&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume266en_US
dc.identifier.issue2en_US
dc.identifier.spage472en_US
dc.identifier.epage480en_US
dc.identifier.isiWOS:000084583100033-
dc.publisher.placeUnited Statesen_US

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