PubMed · 4701857
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1973-04-07. Cell membranes.. https://pubmed.ncbi.nlm.nih.gov/4701857/
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Manganese superoxide dismutase (MnSOD) has been found to be low in a wide range of tumor cells as well as in vitro-transformed cell lines and has been implicated as a new type of tumor suppressor gene. The relationship between MnSOD activity and the malignant phenotype was studied by transfection of MnSOD cDNA into the SV40-transformed human fibroblast cell line WI-38 VA13 subline 2RA. The integration and expression of the exogenous MnSOD cDNA was confirmed in three selected clones with a 2-3.5-fold increase in MnSOD activity. The effect of elevated expression of MnSOD on the cell phenotype was determined by observing growth characteristics. Compared with the parental and neo control cells, the MnSOD-overexpressing clones had a slower growth rate, lower plating efficiency, increased anchorage dependence, and morphological differences. These changes were correlated strongly with the level of MnSOD activity. The results suggest that an increase of MnSOD activity can reverse part of the malignant phenotype in SV40-transformed human fibroblast cells. A possible mechanism is that overexpression of MnSOD might alter the intracellular redox state by modulation of the balance of reactive oxygen species.
Expression of c-Met, the receptor for hepatocyte growth factor (HGF), and the biological roles of HGF were examined in cultured human glioma cells. All of the 5 glioma cell lines examined expressed c-Met protein as well as the c-met gene. Expression of the c-met gene was also confirmed in a glioblastoma tissue. Three cell lines (MGM-3, U251, KG-1-C) demonstrated chemotactic response to HGF in a dose-dependent manner. The response was not only chemotactic but also chemokinetic as judged by a checkerboard analysis. The amounts of c-Met mRNA and protein were abundant in the cell lines which showed a migratory response to HGF. Moreover, c-Met protein expression was highest in U251 with the highest migratory response to HGF. Among the cell lines, KG-1-C produced notable amounts of HGF protein as well as of c-Met, suggesting that HGF may act in an autocrine fashion in this case. HGF did not act as an apparent growth factor in the glioma cell lines examined. Furthermore, HGF stimulated the production of metalloproteinase, probably gelatinase A, in U251 cells.
Retinoids are important physiological agents that regulate epithelial cell differentiation and proliferation. The importance of these agents in regulating growth, development, and differentiation has led to a search for new retinoid agonists and antagonists. In the present manuscript we show that AGN193109, a retinoid analog, is an efficient antagonist of retinoid action in human cervical epithelial cells. Treatment of ECE16-1 cells with natural or synthetic retinoids reduces cytokeratin K5, K6, K14, K16, and K17 levels, increases cytokeratin K7, K8, and K19 levels, increases retinoic acid receptor-beta (RAR beta) mRNA levels, suppresses proliferation, and alters cell morphology. Co-treatment with AGN193109 prevents these responses. Half-maximal and maximal antagonism is observed at a molar ratio of AGN193109: retinoid agonist of 1:1 and 10:1, respectively. When administered alone AGN193109 has no agonist activity. Thus, AGN193109, which binds to RAR alpha, RAR beta, and RAR gamma with Kd values = 2,2, and 3 nm, respectively, but is unable to bind to the retinoid X receptors, is a highly active antagonist of retinoid action in ECE16-1 cells.