PMID- 2806409
OWN - NLM
STAT- MEDLINE
DCOM- 19891218
LR  - 20190707
IS  - 0014-4827 (Print)
IS  - 0014-4827 (Linking)
VI  - 185
IP  - 1
DP  - 1989 Nov
TI  - Growth modulatory effects of a liver-derived growth inhibitor, transforming 
      growth factor beta 1, and recombinant tumor necrosis factor alpha, in normal and 
      neoplastic cells.
PG  - 247-57
AB  - The growth modulatory effects of a rat liver-derived growth inhibitor (LDGI), 
      transforming growth factor beta 1 (TGF-beta 1), and recombinant tumor necrosis 
      factor (rTNF-alpha) were examined in a variety of liver-derived and 
      nonliver-derived normal and neoplastic cell culture systems. Normal rat liver 
      epithelial (RLE) cells were highly sensitive to the growth inhibitory effects of 
      LDGI (ID50 = 0.2 ng/ml) and TGF-beta 1 (ID50 = 0.25 ng/ml) but were less 
      sensitive to rTNF-alpha (ID40 = 5000 Units/ml). Aflatoxin B1-transformed RLE 
      cells showed sensitivity to the cytostatic effects of LDGI (ID50 = 1.5 ng/ml); 
      however, these cells were completely resistant to the antiproliferative effects 
      of TGF-beta 1 and rTNF-alpha. Clones isolated from these transformed cells, 
      exhibited a wide range of sensitivities to LDGI but all of the clones were 
      resistant to the growth inhibitory effects of both TGF-beta 1 and rTNF-alpha. Rat 
      hepatoma Reuber cells were extremely sensitive to the antiproliferative effects 
      of rTNF-alpha (ID50 = 10 Units/ml) but exhibited sensitivity to LDGI only at 
      concentrations above 1.5 ng/ml and were resistant to the antiproliferative 
      effects of TGF-beta 1. Rat hepatoma UVM 7777 cells and human hepatoma HepG2 
      cells, however, were insensitive to the growth inhibitory effects of all three 
      factors. Among the nonliver-derived cells, human breast carcinoma (MCF-7) cells 
      were extremely sensitive to rTNF-alpha (ID50 = 20 Units/ml, exhibited some 
      sensitivity to LDGI (ID50 = 1 ng/ml), and were resistant to the antiproliferative 
      effects of TGF-beta 1. In contrast, the rate of DNA synthesis is rat kidney 
      fibroblasts and human foreskin fibroblasts was significantly stimulated in 
      response to TGF-beta 1, LDGI, and rTNF-alpha. These data demonstrate that LDGI, 
      TGF-beta 1, and rTNF-alpha exert positive and negative modulations of growth in 
      different cell systems and that the growth regulatory effects of LDGI differ from 
      those of TGF-beta 1 and rTNF-alpha in some cell types.
FAU - Chapekar, M S
AU  - Chapekar MS
AD  - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892.
FAU - Huggett, A C
AU  - Huggett AC
FAU - Thorgeirsson, S S
AU  - Thorgeirsson SS
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Exp Cell Res
JT  - Experimental cell research
JID - 0373226
RN  - 0 (Growth Inhibitors)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 76057-06-2 (Transforming Growth Factors)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Animals
MH  - Breast Neoplasms/pathology
MH  - Cell Division/drug effects
MH  - Cell Line
MH  - Cell Transformation, Neoplastic/drug effects/pathology
MH  - Cells, Cultured
MH  - DNA/biosynthesis
MH  - Epithelium/drug effects/pathology
MH  - Female
MH  - Fibroblasts/cytology/drug effects
MH  - Growth Inhibitors/analysis/*pharmacology
MH  - Humans
MH  - Kidney/cytology/drug effects
MH  - Liver/analysis/drug effects/*pathology
MH  - Liver Neoplasms/*pathology
MH  - Male
MH  - Rats
MH  - Recombinant Proteins/*pharmacology
MH  - Transforming Growth Factors/*pharmacology
MH  - Tumor Cells, Cultured/drug effects/pathology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1989/11/01 00:00
MHDA- 1989/11/01 00:01
CRDT- 1989/11/01 00:00
PHST- 1989/11/01 00:00 [pubmed]
PHST- 1989/11/01 00:01 [medline]
PHST- 1989/11/01 00:00 [entrez]
AID - 0014-4827(89)90053-0 [pii]
AID - 10.1016/0014-4827(89)90053-0 [doi]
PST - ppublish
SO  - Exp Cell Res. 1989 Nov;185(1):247-57. doi: 10.1016/0014-4827(89)90053-0.