Abstract
The influence of all trans-retinoic acid on cyclic AMP metabolism was examined in B16-F1 mouse melanoma cells. Treatment of these cells with retinoic acid resulted in a dose-dependent inhibition of cell growth which was accompanied by a concentration-dependent increase in both basal and cyclic AMP-stimulated protein kinase activity, Intracellular levels of cyclic AMP, however, were not altered by retinoid treatment. A protein kinase-deficient variant of B16-F1 (MR-4) did not exhibit decreased growth or increased protein kinase activity in response to retinoic acid treatment. At least 24 h of incubation was required before increased protein kinase activity could be detected in treated B16-F1 cells. Retinoic acid treatment increased the Vmax of protein kinase, but the Ka for cyclic AMP activation was not altered. These findings suggest that in B16 mouse melanoma cells, cyclic AMP-dependent protein kinase may be a target for the growth inhibitory effects of the retinoid.
Highlights
B16-FI cells were obtained through the courtesyof Dr I
Protein kinase activity in control and retinoic acid-treated cells wasassayed by the method of Corbin et al [15]. using a 10-min not exhibit decreased growth or increased protein kinase activity in response to retinoic acid treatment
After 48 h of incubation with 10 ~ L Mretinoic acid, protein kinase activity was assayed as described in the text
Summary
B16-FI cells were obtained through the courtesyof Dr I. From the Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts 02118 serum (heat-inactivated, GIBCO), and incubated in a 37”C, 95% air, 5% CO2 humidified atmosphere Growth inhibition in both cell lines was determined by seeding 2.0 X lo5cells onto 90-mm tissue culture dishes (Falcon, Oxnard,Calif.). The influence of all trans-retinoic acid on cyclic AMP metabolism was examined in Bl6-FI mouse melanoma cells. Protein kinase activity in control and retinoic acid-treated cells wasassayed by the method of Corbin et al [15]. Retinoic acid treatment increased the V,, of protein kinase, but the K,,for cyclic AMP activation was not altered. These findings suggest that in B16 mouse melanoma cells, cyclic AMP-dependent protein kinase may be atarget for the growth inhibitory effects of the retinoid. Cytoplasmic bindingproteins for retinol and retinoic acid have been found in many cell types, itis not understood
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
