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Article: Suppression of the tumorigenicity of mutant p53-transformed rat embryo fibroblasts through expression of a newly cloned rat nonmuscle myosin heavy chain-B

TitleSuppression of the tumorigenicity of mutant p53-transformed rat embryo fibroblasts through expression of a newly cloned rat nonmuscle myosin heavy chain-B
Authors
KeywordsCytoskeletal protein
Mutant p53
nmMHC
Rat 6
Tumor suppression
Issue Date2001
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2001, v. 20 n. 1, p. 58-68 How to Cite?
AbstractIn our previous study, a rat homolog of human nonmuscle myosin heavy chain-B (nmMHC-B) was identified by mRNA differential display comparing of transformed against nontransformed Rat 6 cells over-expressing mutant p53vaI135 gene. The nmMHC-B was found to be expressed in normal Rat 6 embryo fibroblast cell line, but markedly suppressed in the mutant p53vaI135-transformed Rat 6 cells. To examine the possible involvement of nmMHC-B in cell transformation, we first cloned and sequenced the full length cDNA of rat nmMHC-B, which was then cloned into an ecdysone-expression vector. The resulting construct was introduced into the T2 cell line, a mutant p53vaI135-transformed Rat 6 cells lacking the expression of the endogenous nmMHC-B. The clonal transfectants, expressing muristerone A-induced nmMHC-B, displayed a slightly flatter morphology and reached to a lower saturation density compared to the parental transformed cells. Reconstitution of actin filamental bundles was also clearly seen in cells over-expressing the nmMHC-B. In soft agar assays, nmMHC-B transfectants formed fewer and substantially smaller colonies than the parental cells in response to muristerone A induction. Moreover, it was strikingly effective in suppressing the tumorigenicity of the T2 cells when tested in nude mice. Thus, the nmMHC-B, known as a component of the cytoskeletal network, may act as a tumor suppressor gene. Our current finding may reveal a novel role of nmMHC-B in regulating cell growth and cell signaling in nonmuscle cells.
Persistent Identifierhttp://hdl.handle.net/10722/48653
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYam, JWPen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorHsiao, WLWen_HK
dc.date.accessioned2008-05-22T04:20:18Z-
dc.date.available2008-05-22T04:20:18Z-
dc.date.issued2001en_HK
dc.identifier.citationOncogene, 2001, v. 20 n. 1, p. 58-68en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48653-
dc.description.abstractIn our previous study, a rat homolog of human nonmuscle myosin heavy chain-B (nmMHC-B) was identified by mRNA differential display comparing of transformed against nontransformed Rat 6 cells over-expressing mutant p53vaI135 gene. The nmMHC-B was found to be expressed in normal Rat 6 embryo fibroblast cell line, but markedly suppressed in the mutant p53vaI135-transformed Rat 6 cells. To examine the possible involvement of nmMHC-B in cell transformation, we first cloned and sequenced the full length cDNA of rat nmMHC-B, which was then cloned into an ecdysone-expression vector. The resulting construct was introduced into the T2 cell line, a mutant p53vaI135-transformed Rat 6 cells lacking the expression of the endogenous nmMHC-B. The clonal transfectants, expressing muristerone A-induced nmMHC-B, displayed a slightly flatter morphology and reached to a lower saturation density compared to the parental transformed cells. Reconstitution of actin filamental bundles was also clearly seen in cells over-expressing the nmMHC-B. In soft agar assays, nmMHC-B transfectants formed fewer and substantially smaller colonies than the parental cells in response to muristerone A induction. Moreover, it was strikingly effective in suppressing the tumorigenicity of the T2 cells when tested in nude mice. Thus, the nmMHC-B, known as a component of the cytoskeletal network, may act as a tumor suppressor gene. Our current finding may reveal a novel role of nmMHC-B in regulating cell growth and cell signaling in nonmuscle cells.en_HK
dc.format.extent82958 bytes-
dc.format.extent3021 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypetext/plain-
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCytoskeletal proteinen_HK
dc.subjectMutant p53en_HK
dc.subjectnmMHCen_HK
dc.subjectRat 6en_HK
dc.subjectTumor suppressionen_HK
dc.titleSuppression of the tumorigenicity of mutant p53-transformed rat embryo fibroblasts through expression of a newly cloned rat nonmuscle myosin heavy chain-Ben_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0950-9232&volume=20)1)&spage=58&epage=68&date=2000&atitle=Suppression+of+the+tumorigenicity+of+mutant+p53-transformed+rat+embryo+fibroblasts+through+expression+of+a+newly+cloned+rat+nonmuscle+myosin+heavy+chain-Ben_HK
dc.identifier.emailYam, JWP:judyyam@pathology.hku.hken_HK
dc.identifier.authorityYam, JWP=rp00468en_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1038/sj.onc.1203982en_HK
dc.identifier.pmid11244504-
dc.identifier.scopuseid_2-s2.0-0035804225en_HK
dc.identifier.hkuros56450-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035804225&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume20en_HK
dc.identifier.issue1en_HK
dc.identifier.spage58en_HK
dc.identifier.epage68en_HK
dc.identifier.isiWOS:000166361400007-
dc.publisher.placeUnited Kingdomen_HK

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