PMID- 10925356
OWN - NLM
STAT- MEDLINE
DCOM- 20000816
LR  - 20160303
IS  - 0020-7136 (Print)
IS  - 0020-7136 (Linking)
VI  - 87
IP  - 5
DP  - 2000 Sep 1
TI  - u-PA and c-MET mRNA expression is co-ordinately enhanced while hepatocyte growth 
      factor mRNA is down-regulated in human hepatocellular carcinoma.
PG  - 644-9
AB  - Hepatocyte growth factor/scatter factor (HGF/SF) is one of the most important 
      humoral mediators of liver regeneration. It is potentially related to molecular 
      mechanisms of hepatocarcinogenesis via a paracrine system involving its cellular 
      receptor, c-met. In this study, the expression patterns of HGF and c-met were 
      evidenced by multiplex RT-PCR in different specimens of human hepatic tissues (n 
      = 71). A significant increase of c-met mRNA expression was detected in hepatitis 
      (P = 0.001), cirrhosis (P = 0.006), and hepatocellular carcinoma (HCC) tissue (P 
      = 0.003) compared with normal parenchyma and steatosis. HGF mRNA expression was 
      significantly higher only in hepatitis (P = 0.01). Over-expression of c-met mRNA 
      and under-expression of HGF mRNA were detected in the HCCs compared with the 
      corresponding peri-tumoral tissues. Neither HGF nor c-met expression was related 
      to age, sex, tumor size, grading, presence of pseudocapsula, and proliferative 
      activity of the malignant hepatocytes. A significant inverse correlation was 
      found between c-met mRNA expression level and survival (in months) of patients (P 
      = 0.007), as previously shown for urokinase-type plasminogen activator (u-PA) 
      mRNA (P = 0.027). In addition, c-met mRNA expression was strictly associated with 
      u-PA mRNA level in HCC samples (P = 0.001). These data show that a loss of 
      balance concerning HGF, c-met, and u-PA mRNA expression occurs during 
      hepatocarcinogenesis. Particularly, up-regulation of c-met and u-PA mRNA 
      transcription appears to be coordinately regulated, and their levels of 
      expression are inversely correlated with survival; they must therefore play an 
      important role in the development and progression of human HCC and may also be 
      relevant prognostic markers.
CI  - Copyright 2000 Wiley-Liss, Inc.
FAU - Tavian, D
AU  - Tavian D
AD  - Division of Biology and Genetics, Department of Biomedical Sciences and 
      Biotechnology, University of Brescia, Brescia, Italy.
FAU - De Petro, G
AU  - De Petro G
FAU - Benetti, A
AU  - Benetti A
FAU - Portolani, N
AU  - Portolani N
FAU - Giulini, S M
AU  - Giulini SM
FAU - Barlati, S
AU  - Barlati S
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Int J Cancer
JT  - International journal of cancer
JID - 0042124
RN  - 0 (Antigens, Nuclear)
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Fibronectins)
RN  - 0 (Nuclear 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 3.4.21.73 (Urokinase-Type Plasminogen Activator)
SB  - IM
MH  - Antigens, Nuclear
MH  - Biomarkers, Tumor/biosynthesis/genetics
MH  - Carcinoma, Hepatocellular/genetics/*metabolism/pathology
MH  - Cell Division/physiology
MH  - Down-Regulation
MH  - Fibronectins/biosynthesis/genetics
MH  - Gene Expression
MH  - Gene Expression Regulation, Neoplastic
MH  - Hepatitis/genetics/metabolism
MH  - Hepatocyte Growth Factor/*biosynthesis/genetics
MH  - Humans
MH  - Liver/metabolism
MH  - Liver Cirrhosis/genetics/metabolism
MH  - Liver Neoplasms/genetics/*metabolism/pathology
MH  - Nuclear Proteins/metabolism
MH  - Proto-Oncogene Proteins c-met/*biosynthesis/genetics
MH  - RNA, Messenger/*biosynthesis/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Survival Analysis
MH  - Urokinase-Type Plasminogen Activator/*biosynthesis/genetics
EDAT- 2000/08/05 11:00
MHDA- 2000/08/19 11:00
CRDT- 2000/08/05 11:00
PHST- 2000/08/05 11:00 [pubmed]
PHST- 2000/08/19 11:00 [medline]
PHST- 2000/08/05 11:00 [entrez]
AID - 10.1002/1097-0215(20000901)87:5<644::AID-IJC4>3.0.CO;2-W [pii]
PST - ppublish
SO  - Int J Cancer. 2000 Sep 1;87(5):644-9.