The role of the cyclin-dependent kinase inhibitor p21 in apoptosis.
Andrei L. Gartela, Angela L. Tynerb
- aDepartment of Molecular Genetics, University of Illinois College of Medicine, Chicago, Illinois 60607, USA. agartel@uic.edu
- bBiochem & Molecular Genetics
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Abstract
Cancer develops when the balance between cell proliferation and cell death is disrupted, and the ensuing aberrant proliferation leads to tumor growth. The cyclin-dependent kinase inhibitor p21 is induced by both p53-dependent and -independent mechanisms following stress, and induction of p21 may cause cell cycle arrest. As a proliferation inhibitor, p21 is poised to play an important role in preventing tumor development. This notion is supported by data indicating that p21-null mice are more prone to spontaneous and induced tumorigenesis, and p21 synergizes with other tumor suppressors to protect against tumor progression in mice. However, a number of recent studies have pointed out that in addition to being an inhibitor of cell proliferation, p21 acts as an inhibitor of apoptosis in a number of systems, and this may counteract its tumor-suppressive functions as a growth inhibitor. In the current review, we discuss the role of p21 in regulating cell death and the potential relevance of its expression in cancer.
TL;DRThe role of p21 in regulating cell death and the potential relevance of its expression in cancer are discussed and this may counteract its tumor-suppressive functions as a growth inhibitor. (Semantic Scholar)