| Abstract: |
Findings of increased numbers of epidermal growth factor receptors (EGF-R) and increased expression of transforming growth factor a (TGF-α) in surgical specimens of human renal cell carcinoma have led to the proposal that growth of these tumors may be regulated by TGF-α in an autocrine manner. In the studies presented here, we have examined this hypothesis using two human renal carcinoma cell lines, SKRC-4 and SKRC-29. We demonstrated that both SKRC-4 and SKRC-29 cells were growth stimulated by >35% when cultured in the presence of TGF-α or EGF and were inhibited by 29% to 46% if cultured in the presence of anti-EGF-R monoclonal antibody 225. Treatment of cells with TGF-α enhanced the levels of expression of EGF-R mRNA and TGF-α mRNA. In addition, incubation of cells with monoclonal antibody 225 significantly elevated the levels of excreted TGF-α species in the culture medium. Our findings suggest that proliferation of human renal carcinoma cells may be regulated by endogenously produced TGF-α and that this regulatory pathway can be interrupted using antibody to its receptor, EGF-R. © 1992, American Association for Cancer Research. All rights reserved. |
| Keywords: |
epidermal growth factor; human cell; cell division; cell growth; epidermal growth factor receptor; receptor, epidermal growth factor; tumor cells, cultured; kidney carcinoma; monoclonal antibody; rna; isotope labeling; carcinoma, renal cell; rna, messenger; growth regulation; immunoprecipitation; immunoblotting; protein induction; carcinoma cell; receptor binding; transforming growth factor alpha; rna analysis; receptor upregulation; growth stimulation; sulfur 35; human; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.
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