PMID- 7907335
OWN - NLM
STAT- MEDLINE
DCOM- 19940414
LR  - 20131121
IS  - 0730-2312 (Print)
IS  - 0730-2312 (Linking)
VI  - 54
IP  - 1
DP  - 1994 Jan
TI  - Differential regulation of tissue transglutaminase in rat hepatoma cell lines 
      McA-RH7777 and McA-RH8994: relation to growth rate and cell death.
PG  - 67-77
AB  - Close correlation between tissue transglutaminase (tTG) induction and growth 
      regulation and/or cell death processes has been suggested in many cell lineages. 
      In this study, the regulation of the tTG levels by various growth and 
      differentiation factors and its relation to growth rate and cell death processes 
      were investigated in two rat hepatoma cell lines, McA-RH7777 and McA-RH8994, 
      using a monoclonal antibody against liver tTG. Transforming growth factor-beta 1 
      (TGF-beta 1) and retinoic acid (RA) each increased tTG to the level of 8- to 
      32-fold above that of control cultures in both cell lines after 72-h treatment. 
      Dexamethasone (DEX) induced a 16- to 32-fold of tTG in McA-RH8994 cells while it 
      did not change the enzyme level in McA-RH7777 cells. Simultaneous addition of DEX 
      and RA increased the tTG level to more than 50-fold in McA-RH7777 cells as well 
      as McA-RH8994 cells. Other factors, such as TGF-alpha, hepatocyte growth factor, 
      dimethyl sulfoxide, and protein kinase C activator, did not show significant 
      increases of the tTG levels. Although tTG induction by TGF-beta 1 or DEX appeared 
      to be correlated with their growth suppressive effects, RA increased the tTG 
      level without suppressing the growth rate of hepatoma cells. TGF-beta 1 was also 
      shown to induce cell death in both cell lines. Our results demonstrate that RA 
      and DEX are capable of modulating the TGF-beta 1-induced cell death processes 
      independent of the tTG levels. We present evidence here that tTG induction by 
      itself is not the direct cause of growth suppression and cell death in these 
      hepatoma cells.
FAU - Fukuda, K
AU  - Fukuda K
AD  - First Department of Pathology, Kurume University School of Medicine, Japan.
FAU - Kojiro, M
AU  - Kojiro M
FAU - Chiu, J F
AU  - Chiu JF
LA  - eng
GR  - NCI CA25098/CA/NCI NIH HHS/United States
GR  - NCI CA42965/CA/NCI NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Transforming Growth Factor beta)
RN  - 5688UTC01R (Tretinoin)
RN  - 7S5I7G3JQL (Dexamethasone)
RN  - EC 2.3.2.13 (Transglutaminases)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/pharmacology
MH  - Blotting, Northern
MH  - *Cell Death/drug effects
MH  - *Cell Division/drug effects
MH  - Dexamethasone/pharmacology
MH  - Drug Interactions
MH  - Liver Neoplasms, Experimental/*enzymology/pathology
MH  - Rats
MH  - Transforming Growth Factor beta/pharmacology
MH  - Transglutaminases/immunology/*metabolism
MH  - Tretinoin/pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
AID - 10.1002/jcb.240540108 [doi]
PST - ppublish
SO  - J Cell Biochem. 1994 Jan;54(1):67-77. doi: 10.1002/jcb.240540108.