PMID- 9535822
OWN - NLM
STAT- MEDLINE
DCOM- 19980514
LR  - 20161124
IS  - 0006-291X (Print)
IS  - 0006-291X (Linking)
VI  - 245
IP  - 1
DP  - 1998 Apr 7
TI  - Induction of apoptosis by hepatocyte growth factor/scatter factor and its 
      augmentation by phorbol esters in Meth A cells.
PG  - 278-83
AB  - Hepatocyte growth factor/scatter factor (HGF/SF) is a multifunctional cytokine 
      with mitogenic, motogenic, and morphogenic activities. In addition, HGF/SF 
      inhibits the proliferation of some tumor cell lines, but its mechanism remains 
      poorly understood. We determined in this study whether HGF/SF induces cell death 
      of a Meth A mouse sarcoma cell line in vitro, whose proliferation is remarkably 
      suppressed by HGF/SF. Inhibition of Meth A cell growth by HGF/SF was 
      dose-dependent and maximal at a concentration of 30 ng/ml. The percentage of dead 
      cells increased to 22% upon treatment with 30 ng/ml of HGF/SF for 96 h, whereas 
      that in untreated cultures was less than 5%. Staining of these cells nuclei with 
      Hoechst 33342 revealed condensation of the chromatin and nuclear fragmentation. 
      Gel electrophoresis of DNA from HGF/SF-treated cells showed a typical ladder 
      pattern. Cells with a fractional DNA content also increased five-fold in the 
      HGF/SF-treated cultures as analyzed by flow cytometry after propidium iodide 
      staining. These are features typical of apoptosis. Concurrent addition of 
      12-O-tetradecanoylphorbol 13-acetate (TPA) with HGF/SF augmented the apoptosis 
      induced by the growth factor, while TPA alone caused little death. This 
      enhancement was largely blocked by addition of the specific protein kinase C 
      inhibitor GF 109203X. These results indicate that HGF/SF induced the apoptotic 
      cell death of the Meth A sarcoma cell line and that protein kinase C activation 
      augmented the growth factor-induced apoptosis.
CI  - Copyright 1998 Academic Press.
FAU - Gohda, E
AU  - Gohda E
AD  - Department of Immunochemistry, Faculty of Pharmaceutical Sciences, Okayama 
      University, Tsushima-naka, Okayama, 700-8530, Japan. 
      gohda@pheasant.pharm.okayama-u.ac.jp
FAU - Okauchi, H
AU  - Okauchi H
FAU - Iwao, M
AU  - Iwao M
FAU - Yamamoto, I
AU  - Yamamoto I
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Benzimidazoles)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Indoles)
RN  - 0 (Maleimides)
RN  - 67256-21-7 (Hepatocyte Growth Factor)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - L79H6N0V6C (bisindolylmaleimide I)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
RN  - P976261J69 (bisbenzimide ethoxide trihydrochloride)
SB  - IM
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Benzimidazoles/metabolism
MH  - Cell Cycle/physiology
MH  - Cell Survival/drug effects
MH  - DNA Fragmentation/drug effects
MH  - DNA Replication/drug effects
MH  - Flow Cytometry
MH  - Fluorescent Dyes/metabolism
MH  - Hepatocyte Growth Factor/*pharmacology
MH  - Indoles/pharmacology
MH  - Maleimides/pharmacology
MH  - Mice
MH  - Protein Kinase C/antagonists & inhibitors
MH  - Tetradecanoylphorbol Acetate/*pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1998/05/16 00:00
MHDA- 1998/05/16 00:01
CRDT- 1998/05/16 00:00
PHST- 1998/05/16 00:00 [pubmed]
PHST- 1998/05/16 00:01 [medline]
PHST- 1998/05/16 00:00 [entrez]
AID - S0006-291X(98)98416-9 [pii]
AID - 10.1006/bbrc.1998.8416 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 1998 Apr 7;245(1):278-83. doi: 
      10.1006/bbrc.1998.8416.