Abstract
The effects of corticotropin-releasing factor (CRF) on human lung cancer cell lines was investigated. Corticotropin-releasing factor increased the cAMP levels in a dose-dependent manner; CRF (100 n M) elevated the cAMP levels approximately elevenfold using NCI-H345 cells and increased the gastrin-releasing peptide (GRP) secretion rate by approximately 70%. Similarly, sauvagine, a structural analogue of CRF, elevated the cAMP levels with a half-maximal effective dose (ED 50) of 20 n M. The increase in cAMP caused by CRF and sauvagine was reversed by α-helical CRF(9–41). Corticotropin-releasing factor had no effect on cytosolic calcium but stimulated [ 3H]arachidonic acid release from NCI-H1299 cells with an ED 50 of 30 n M. The increase in [ 3H]arachidonic acid release caused by 100 n M CRF was significantly reversed by 1 or 10 μ M α-helical CRF(9–41). Also, CRF stimulated the clonal growth of NCI-H345 and H720 cells and the growth increase caused by CRF was reversed by α-helical CRF(9–41). These data suggest that CRF may be a regulatory peptide in lung cancer.
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