Lack of mda-6/WAF1/CIP1-mediated inhibition of cyclin-dependent kinases in interferon-α resistant murine B16 melanoma cells
Previously we demonstrated that IFN-α augments mda-6/WAF1 and inhibits cyclin-dependent kinases in a p53-independent fashion in B16 murine melanoma cells. On the other hand, IFN-γ activates p53 expression without affecting the mda-6/WAF1 system. Combination of the two IFNs is additive. B16 cells acq...
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Published in | Cancer letters Vol. 119; no. 2; pp. 237 - 240 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Shannon
Elsevier Ireland Ltd
11.11.1997
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Previously we demonstrated that IFN-α augments mda-6/WAF1 and inhibits cyclin-dependent kinases in a p53-independent fashion in B16 murine melanoma cells. On the other hand, IFN-γ activates p53 expression without affecting the mda-6/WAF1 system. Combination of the two IFNs is additive. B16 cells acquire IFN-α resistant but IFN-γ sensitive phenotype after long term IFN-α treatment (B16α cells). Here we demonstrate the absence of mda-6/WAF1-associated repression of cyclindependent kinases, but the existence of p53-dependent c-
myc inhibition in IFN-γ-treated B16α cells. Clearly, selective desensitization of IFN-α related growth regulation does not influence the IFN-γ associated pathway. Our results further support the coexistence of distinct growth regulatory mechanisms in B16 cells that can be activated by different IFN-types independently of each other. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0304-3835 1872-7980 |
DOI: | 10.1016/S0304-3835(97)00288-7 |