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Article: Aberrant expression of hepatocyte growth factor and its receptor, c-Met, during sex hormone-induced prostatic carcinogenesis in the Noble rat
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TitleAberrant expression of hepatocyte growth factor and its receptor, c-Met, during sex hormone-induced prostatic carcinogenesis in the Noble rat
 
AuthorsTam, NNC1
Chung, SSM1
Lee, DTW1
Wong, YC1
 
Issue Date2000
 
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
CitationCarcinogenesis, 2000, v. 21 n. 12, p. 2183-2191 [How to Cite?]
 
AbstractHepatocyte growth factor (HGF) is a multifunctional cytokine which acts as a mitogen, motogen, morphogen and angiogenic factor of epithelial cells. HGF receptor is encoded by a proto-oncogene, c-met, which is overexpressed in various cancers. The role of HGF and c-Met in prostate carcinogenesis, especially in the early stages, is undefined. In this study, prostatic dysplasia and carcinomas were induced by testosterone propionate and 17β-estradiol in Noble rats. The expression of HGF and c-Met was assessed at a protein level by immunohistochemistry and western blot analysis. Intense immunostaining for HGFα and c-Met β-chain was co-localized in dysplastic lesions and in primary and metastatic cancer cells. The levels of HGFα expression were similar among normal control, dysplastic and cancerous prostate tissues, as determined by western blot analysis. Immunoblot study for c-Met under reducing conditions identified two bands at 145 kDa (β-subunit of c-Met) and 170 kDa (precursor form of c-Met) in rat liver extracts. However, two bands at Ο220 and 245 kDa were detected in hormone-treated dysplastic prostate tissues and primary tumors. Overexpression of the 220 kDa band was observed in long-term (10-12 months) hormone-treated prostate and primary tumor extracts. Metastatic tumors consistently exhibited up-regulation of a single 245 kDa band. Under non-reducing conditions, however, protein bands of 220, 280 or 300 kDa were seen in the blots. The hormone-treated prostate tissues and metastatic tumors expressed the 220 and 300 kDa proteins, respectively. The majority of primary tumors expressed the 280 kDa protein. In summary, HGF and its receptor, c-Met, were co-expressed in dysplastic and tumor cells, suggesting that an autocrine mode of action may be involved in prostate carcinogenesis. The close correlation of expression of the high-molecular-weight isoforms of c-Met with different stages of carcinogenesis implicates that they might play differential roles in the onset, progression, growth and metastasis in prostate cancer.
 
ISSN0143-3334
2012 Impact Factor: 5.635
2012 SCImago Journal Rankings: 2.349
 
ISI Accession Number IDWOS:000166347100007
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorTam, NNC
 
dc.contributor.authorChung, SSM
 
dc.contributor.authorLee, DTW
 
dc.contributor.authorWong, YC
 
dc.date.accessioned2010-09-06T05:57:05Z
 
dc.date.available2010-09-06T05:57:05Z
 
dc.date.issued2000
 
dc.description.abstractHepatocyte growth factor (HGF) is a multifunctional cytokine which acts as a mitogen, motogen, morphogen and angiogenic factor of epithelial cells. HGF receptor is encoded by a proto-oncogene, c-met, which is overexpressed in various cancers. The role of HGF and c-Met in prostate carcinogenesis, especially in the early stages, is undefined. In this study, prostatic dysplasia and carcinomas were induced by testosterone propionate and 17β-estradiol in Noble rats. The expression of HGF and c-Met was assessed at a protein level by immunohistochemistry and western blot analysis. Intense immunostaining for HGFα and c-Met β-chain was co-localized in dysplastic lesions and in primary and metastatic cancer cells. The levels of HGFα expression were similar among normal control, dysplastic and cancerous prostate tissues, as determined by western blot analysis. Immunoblot study for c-Met under reducing conditions identified two bands at 145 kDa (β-subunit of c-Met) and 170 kDa (precursor form of c-Met) in rat liver extracts. However, two bands at Ο220 and 245 kDa were detected in hormone-treated dysplastic prostate tissues and primary tumors. Overexpression of the 220 kDa band was observed in long-term (10-12 months) hormone-treated prostate and primary tumor extracts. Metastatic tumors consistently exhibited up-regulation of a single 245 kDa band. Under non-reducing conditions, however, protein bands of 220, 280 or 300 kDa were seen in the blots. The hormone-treated prostate tissues and metastatic tumors expressed the 220 and 300 kDa proteins, respectively. The majority of primary tumors expressed the 280 kDa protein. In summary, HGF and its receptor, c-Met, were co-expressed in dysplastic and tumor cells, suggesting that an autocrine mode of action may be involved in prostate carcinogenesis. The close correlation of expression of the high-molecular-weight isoforms of c-Met with different stages of carcinogenesis implicates that they might play differential roles in the onset, progression, growth and metastasis in prostate cancer.
 
dc.description.naturelink_to_OA_fulltext
 
dc.identifier.citationCarcinogenesis, 2000, v. 21 n. 12, p. 2183-2191 [How to Cite?]
 
dc.identifier.epage2191
 
dc.identifier.hkuros56508
 
dc.identifier.isiWOS:000166347100007
 
dc.identifier.issn0143-3334
2012 Impact Factor: 5.635
2012 SCImago Journal Rankings: 2.349
 
dc.identifier.issue12
 
dc.identifier.openurl
 
dc.identifier.pmid11133807
 
dc.identifier.scopuseid_2-s2.0-0034526646
 
dc.identifier.spage2183
 
dc.identifier.urihttp://hdl.handle.net/10722/67656
 
dc.identifier.volume21
 
dc.languageeng
 
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofCarcinogenesis
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCarcinogenesis. Copyright © Oxford University Press.
 
dc.subject.meshAnimals
 
dc.subject.meshBlotting, Western
 
dc.subject.meshHepatocyte Growth Factor - analysis - genetics
 
dc.subject.meshImmunohistochemistry
 
dc.subject.meshMale
 
dc.subject.meshMolecular Weight
 
dc.subject.meshNeoplasm Metastasis
 
dc.subject.meshPrecancerous Conditions - chemically induced - genetics - pathology
 
dc.subject.meshProstate - drug effects - metabolism - pathology
 
dc.subject.meshProstatic Neoplasms - chemically induced - genetics - pathology
 
dc.subject.meshProtein Subunits
 
dc.subject.meshProto-Oncogene Proteins c-met - analysis - genetics
 
dc.subject.meshRats
 
dc.subject.meshRats, Inbred Strains
 
dc.subject.meshTestosterone - toxicity
 
dc.subject.meshTime Factors
 
dc.titleAberrant expression of hepatocyte growth factor and its receptor, c-Met, during sex hormone-induced prostatic carcinogenesis in the Noble rat
 
dc.typeArticle
 
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<description.abstract>Hepatocyte growth factor (HGF) is a multifunctional cytokine which acts as a mitogen, motogen, morphogen and angiogenic factor of epithelial cells. HGF receptor is encoded by a proto-oncogene, c-met, which is overexpressed in various cancers. The role of HGF and c-Met in prostate carcinogenesis, especially in the early stages, is undefined. In this study, prostatic dysplasia and carcinomas were induced by testosterone propionate and 17&#946;-estradiol in Noble rats. The expression of HGF and c-Met was assessed at a protein level by immunohistochemistry and western blot analysis. Intense immunostaining for HGF&#945; and c-Met &#946;-chain was co-localized in dysplastic lesions and in primary and metastatic cancer cells. The levels of HGF&#945; expression were similar among normal control, dysplastic and cancerous prostate tissues, as determined by western blot analysis. Immunoblot study for c-Met under reducing conditions identified two bands at 145 kDa (&#946;-subunit of c-Met) and 170 kDa (precursor form of c-Met) in rat liver extracts. However, two bands at &#927;220 and 245 kDa were detected in hormone-treated dysplastic prostate tissues and primary tumors. Overexpression of the 220 kDa band was observed in long-term (10-12 months) hormone-treated prostate and primary tumor extracts. Metastatic tumors consistently exhibited up-regulation of a single 245 kDa band. Under non-reducing conditions, however, protein bands of 220, 280 or 300 kDa were seen in the blots. The hormone-treated prostate tissues and metastatic tumors expressed the 220 and 300 kDa proteins, respectively. The majority of primary tumors expressed the 280 kDa protein. In summary, HGF and its receptor, c-Met, were co-expressed in dysplastic and tumor cells, suggesting that an autocrine mode of action may be involved in prostate carcinogenesis. The close correlation of expression of the high-molecular-weight isoforms of c-Met with different stages of carcinogenesis implicates that they might play differential roles in the onset, progression, growth and metastasis in prostate cancer.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong