PMID- 9221809
OWN - NLM
STAT- MEDLINE
DCOM- 19970724
LR  - 20220321
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 74
IP  - 3
DP  - 1997 Jun 20
TI  - Expression of the c-Met/HGF receptor in human breast carcinoma: correlation with 
      tumor progression.
PG  - 301-9
AB  - Hepatocyte growth factor/scatter factor (HGF/SF) induces cell motility and tissue 
      remodeling of various epithelial cells through its receptor, the product of the 
      proto-oncogene c-met. High levels of HGF/SF have been correlated with poor 
      prognosis in human breast carcinoma. In this study, we examined the expression of 
      the c-Met receptor in human breast-carcinoma cells in vivo and in cultured cell 
      lines. Immunohistochemical analysis of biopsy samples of human breast carcinoma 
      indicated that, in normal mammary gland, c-Met is localized in the ductal 
      epithelium. The level of expression of c-Met in primary carcinomas was maintained 
      in autologous metastatic lymph-node lesions in some cases, and in other cases was 
      elevated. Frequently there was evidence of heterogeneity in cellular expression 
      of c-Met within individual tumors, suggesting that micro-environmental factors 
      may regulate receptor expression. In an analysis of a panel of human 
      breast-carcinoma cell lines, we found that moderately differentiated cell lines 
      did not express detectable levels of c-Met and were not responsive to HGF. In 
      contrast, poorly differentiated and invasive cell lines did express high levels 
      of the receptor and responded to HGF by increased motility and invasiveness. 
      Sensitivity to HGF/SF also correlated with expression of the c-Met 9-kb mRNA. No 
      correlation was found between gene copy number and the expression level of c-Met 
      protein or mRNA. When the moderately differentiated and c-Met-negative T47D cell 
      line was transfected with c-DNA for c-met, the transfectants showed delayed cell 
      scattering and migratory response to HGF. Thus, over-expression of c-Met in 
      moderately differentiated carcinoma cells may be one of several attributes that 
      contribute to an invasive phenotype during the progression of breast cancer.
FAU - Beviglia, L
AU  - Beviglia L
AD  - Department of Stomatology, and the Cardiovascular Research Institute, University 
      of California, San Francisco 94143-0512, USA.
FAU - Matsumoto, K
AU  - Matsumoto K
FAU - Lin, C S
AU  - Lin CS
FAU - Ziober, B L
AU  - Ziober BL
FAU - Kramer, R H
AU  - Kramer RH
LA  - eng
GR  - DE 11436/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (MAS1 protein, human)
RN  - 0 (Proto-Oncogene Mas)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
SB  - IM
MH  - Blotting, Western
MH  - Breast Neoplasms/*metabolism/pathology
MH  - Cell Line, Transformed
MH  - Cell Movement/drug effects
MH  - Disease Progression
MH  - Female
MH  - Hepatocyte Growth Factor/genetics/*metabolism
MH  - Humans
MH  - Neoplasm Invasiveness
MH  - Proto-Oncogene Mas
MH  - Proto-Oncogene Proteins/genetics/*metabolism
MH  - Proto-Oncogene Proteins c-met
MH  - RNA, Messenger/metabolism
MH  - Receptor Protein-Tyrosine Kinases/genetics/*metabolism
MH  - Transcription, Genetic
MH  - Transfection
MH  - Tumor Cells, Cultured
EDAT- 1997/06/20 00:00
MHDA- 2000/06/20 09:00
CRDT- 1997/06/20 00:00
PHST- 1997/06/20 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1997/06/20 00:00 [entrez]
AID - 10.1002/(SICI)1097-0215(19970620)74:3<301::AID-IJC12>3.0.CO;2-E [pii]
AID - 10.1002/(sici)1097-0215(19970620)74:3<301::aid-ijc12>3.0.co;2-e [doi]
PST - ppublish
SO  - Int J Cancer. 1997 Jun 20;74(3):301-9. doi: 
      10.1002/(sici)1097-0215(19970620)74:3<301::aid-ijc12>3.0.co;2-e.