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Tenascin-C induction by the diffusible factor epidermal growth factor in stromal-epithelial interactions
1Division of Hemopoiesis, Jichi Medical School, Tochigi, Japan.
Journal of Cellular Physiology
|October 1, 1995
Summary
Epidermal growth factor (EGF) induces tenascin-C expression in human carcinoma cells, playing a key role in stromal-epithelial interactions during cancer progression. This finding highlights EGF
Area of Science:
- Molecular Biology
- Cell Biology
- Cancer Research
Background:
- Tenascin-C is an extracellular matrix glycoprotein involved in carcinogenesis, invasion, and metastasis.
- Stromal-epithelial interactions are crucial in cancer progression.
- Carcinoma cells may not express tenascin-C in vitro but can do so in vivo or under specific conditions.
Purpose of the Study:
- To investigate the role of growth factors, particularly epidermal growth factor (EGF), in inducing tenascin-C expression in human carcinoma cells.
- To elucidate the mechanisms of tenascin-C induction in the context of stromal-epithelial interactions.
Main Methods:
- Culturing human epidermoid carcinoma cell lines (A431, HEp-2, A549) in vitro and transplanting them into nude mice.
- Treating cells with various growth factors: transforming growth factor beta 1 (TGF-beta 1), EGF, hepatocyte growth factor (HGF), and platelet-derived growth factor (PDGF).
- Co-culturing carcinoma cells with mouse embryonic fibroblasts and using conditioned media.
- Employing antibodies against EGF and its receptor to block signaling pathways.
- Analyzing changes in cytoskeleton and focal contacts using microscopy.
Main Results:
- EGF significantly induced tenascin-C expression in A431 and HEp-2 cells (3.5-fold greater than TGF-beta 1).
- HGF and PDGF had minimal effect on tenascin-C induction.
- EGF also induced fibronectin and laminin expression.
- Co-culture with tenascin-C-null fibroblasts or their conditioned medium induced tenascin-C in carcinoma cells, an effect reduced by anti-EGF antibodies.
- EGF disrupted cytoskeleton and focal contacts in responsive carcinoma cells.
- EGF did not induce tenascin-C or affect morphology in A549 cells, which do not produce tenascin-C after transplantation.
Conclusions:
- Epidermal growth factor (EGF) is a potent inducer of tenascin-C in tenascin-C-nonproducing human carcinoma cells via EGF receptors.
- EGF plays a significant role in stromal-epithelial interactions, mediating tenascin-C induction.
- EGF-induced tenascin-C expression and morphological changes may contribute to cancer cell invasion and metastasis.