| Abstract: |
The CaKi-I line of renal carcinoma (RC) cells is highly sensitive to the antiproliferative effect of human leukocyte interferon (IFN-a). These RC cells express high numbers of cell surface receptors for epidermal growth factor (EGF), and EGF stimulates their proliferation. IFN-a blocks EGF-stimulated proliferation of these cells and down-regulates EGF receptors (EGFR) by inhibiting EGFR synthesis. Although EGF stimulates the proliferation of RC cells resistant to the antiproliferative action of IFN-a, IFN-a treatment does not block the EGF-stimulated proliferation of these cells and has no effect on EGFR expression. Thus, the down-regulation of EGFR is specific for RC cells sensitive to IFN-a. While IFN-a does not affect the level of total cellular message or total polyadenylated message for the EGFR, IFN-a treatment decreases the level of cytoplasmic EGFR message. Analysis of polysome distribution of cellular mRNAs indicates that IFN-a treatment results in an accu mulation of I <.l R mRNA in lighter polysome fractions, consistent with a partial block in translational elongation. Thus, IFN-a regulates the expression of EGFR and possibly other growth-related proteins by posttranscriptional mechanisms, which may play an important part in the complex inhibitory action of IFN-a on RC proliferation. © 1991, American Association for Cancer Research. All rights reserved. |
| Keywords: |
epidermal growth factor; controlled study; human cell; cell division; gene expression; epidermal growth factor receptor; cell line; down-regulation; receptor, epidermal growth factor; dose-response relationship, drug; kidney carcinoma; kidney neoplasms; rna; kinetics; carcinoma, renal cell; rna, messenger; tumor cell line; polyribosomes; down regulation; growth inhibition; recombinant alpha interferon; interferon type i, recombinant; human; priority journal; article; support, non-u.s. gov't; support, u.s. gov't, p.h.s.; poly a; glyceraldehyde-3-phosphate dehydrogenases
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