PMID- 25268161
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20141001
LR  - 20211021
IS  - 2072-6694 (Print)
IS  - 2072-6694 (Electronic)
IS  - 2072-6694 (Linking)
VI  - 6
IP  - 4
DP  - 2014 Sep 29
TI  - Mechanisms of hepatocyte growth factor activation in cancer tissues.
PG  - 1890-904
LID - 10.3390/cancers6041890 [doi]
AB  - Hepatocyte growth factor/scatter factor (HGF/SF) plays critical roles in cancer 
      progression through its specific receptor, MET. HGF/SF is usually synthesized and 
      secreted as an inactive proform (pro-HGF/SF) by stromal cells, such as 
      fibroblasts. Several serine proteases are reported to convert pro-HGF/SF to 
      mature HGF/SF and among these, HGF activator (HGFA) and matriptase are the most 
      potent activators. Increased activities of both proteases have been observed in 
      various cancers. HGFA is synthesized mainly by the liver and secreted as an 
      inactive pro-form. In cancer tissues, pro-HGFA is likely activated by thrombin 
      and/or human kallikrein 1-related peptidase (KLK)-4 and KLK-5. Matriptase is a 
      type II transmembrane serine protease that is expressed by most epithelial cells 
      and is also synthesized as an inactive zymogen. Matriptase activation is likely 
      to be mediated by autoactivation or by other trypsin-like proteases. Recent 
      studies revealed that matriptase autoactivation is promoted by an acidic 
      environment. Given the mildly acidic extracellular environment of solid tumors, 
      matriptase activation may, thus, be accelerated in the tumor microenvironment. 
      HGFA and matriptase activities are regulated by HGFA inhibitor (HAI)-1 (HAI-1) 
      and/or HAI-2 in the pericellular microenvironment. HAIs may have an important 
      role in cancer cell biology by regulating HGF/SF-activating proteases.
FAU - Kawaguchi, Makiko
AU  - Kawaguchi M
AD  - Section of Oncopathology and Regenerative Biology, Department of Pathology, 
      Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 
      889-1692, Japan. kawaguchi@med.miyazaki-u.ac.jp.
FAU - Kataoka, Hiroaki
AU  - Kataoka H
AD  - Section of Oncopathology and Regenerative Biology, Department of Pathology, 
      Faculty of Medicine, University of Miyazaki, 5200 Kihara, Kiyotake, Miyazaki 
      889-1692, Japan. mejina@med.miyazaki-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20140929
PL  - Switzerland
TA  - Cancers (Basel)
JT  - Cancers
JID - 101526829
PMC - PMC4276949
EDAT- 2014/10/01 06:00
MHDA- 2014/10/01 06:01
PMCR- 2014/09/29
CRDT- 2014/10/01 06:00
PHST- 2014/07/02 00:00 [received]
PHST- 2014/09/02 00:00 [revised]
PHST- 2014/09/03 00:00 [accepted]
PHST- 2014/10/01 06:00 [entrez]
PHST- 2014/10/01 06:00 [pubmed]
PHST- 2014/10/01 06:01 [medline]
PHST- 2014/09/29 00:00 [pmc-release]
AID - cancers6041890 [pii]
AID - cancers-06-01890 [pii]
AID - 10.3390/cancers6041890 [doi]
PST - epublish
SO  - Cancers (Basel). 2014 Sep 29;6(4):1890-904. doi: 10.3390/cancers6041890.