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Abstract
Retinoic acid transiently induced expression of high levels of epidermal growth factor receptor (EGFR) in the human non-small cell lung carcinoma cell line H460a. Scatchard analysis revealed a 40-fold increase in the expression of EGFR on the cell surface of H460a cells within 48 h of treatment with 5 mu M concentrations of retinoic acid. RNase protection and nuclear run-off assays established that increases in EGFR expression in retinoic acid-treated cells were not the result of increased promoter activity of EGFR gene, but were more likely the result of a posttranscriptional mechanism. Immune complex kinase assays demonstrated that the EGFR induced by retinoic acid was functionally active. We conclude that retinoic acid exerts its control over expression of the EGFR in H460a cells through a posttranscriptional mechanism. Moreover, elevated EGFR might play a role in the increased tumorigenic potential exhibited by retinoic acid-treated H460a cells.
Published Version
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