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Regulation of cell growth by recombinant oncostatin M
D Horn1, W C Fitzpatrick, P T Gompper
1Oncogen, Seattle, Washington 98121.
Abstract:
Oncostatin M is a novel growth regulator originally isolated from differentiated human histiocytic lymphoma cells and activated T-lymphocytes based on its ability to inhibit the growth of A375 melanoma cells. We report here that oncostatin M is a widely acting regulator which alters the growth and/or morphology of cells derived from a variety of cancer cell types. At picomolar concentrations, recombinant oncostatin M inhibited the growth of 13/24 tumor cell lines. Six out of 7 lung cancer cell lines were inhibited by oncostatin M, but none of 6 colon cancer cell lines were affected. Oncostatin M also stimulated the growth of some normal cells (3/6), indicating that it, like many growth regulators, is bifunctional. Oncostatin M receptors appear necessary but not sufficient for a growth response to oncostatin M, since none of the cell lines lacking receptor responded to oncostatin M, whereas many but not all cell lines with receptor responded to oncostatin M. Receptor size (Mr congruent to 150,000) was similar for cells in which growth was inhibited, stimulated, or unaffected by oncostatin M.
Insights
Oncostatin M (OSM) is a potent regulator that inhibits many cancer cell growth. This bifunctional regulator also stimulates some normal cells, with receptor presence being necessary for a response.
Area of Science:
- Cell Biology
- Molecular Biology
- Cancer Research
Background:
- Oncostatin M (OSM) is a novel growth regulator initially identified for its ability to inhibit melanoma cell growth.
- OSM is derived from differentiated human histiocytic lymphoma cells and activated T-lymphocytes.
Purpose of the Study:
- To investigate the broad regulatory effects of Oncostatin M on various cancer cell types.
- To determine the role of Oncostatin M receptors in mediating cellular responses to OSM.
Main Methods:
- Treatment of multiple cancer and normal cell lines with recombinant Oncostatin M at picomolar concentrations.
- Assessment of cell growth inhibition and morphological changes.
- Analysis of Oncostatin M receptor expression and its correlation with cellular response.
Main Results:
- Recombinant Oncostatin M inhibited the growth of 13 out of 24 tested tumor cell lines, notably 6 out of 7 lung cancer cell lines.
- OSM demonstrated bifunctional activity, inhibiting tumor cell growth while stimulating growth in 3 out of 6 normal cell types.
- Presence of Oncostatin M receptors was essential for any cellular response, though not all receptor-bearing cells responded.
Conclusions:
- Oncostatin M is a widely acting regulator with significant anti-tumor activity against various cancer types, including lung cancer.
- The bifunctional nature of OSM suggests complex roles in both cancer and normal tissue regulation.
- Oncostatin M receptor expression is a prerequisite for OSM-mediated growth modulation, highlighting its importance in signaling pathways.