Please use this identifier to cite or link to this item: https://doi.org/10.3390/cancers11081112
Title: p21cip1/waf1 coordinate autophagy, proliferation and apoptosis in response to metabolic stress
Authors: Manu, K.A.
Cao, P.H.A.
Chai, T.F.
Casey, P.J.
Wang, M. 
Keywords: Apoptosis
Autophagy
Cancer
Cell cycle
Metabolic stress
p21
Issue Date: 2019
Publisher: MDPI AG
Citation: Manu, K.A., Cao, P.H.A., Chai, T.F., Casey, P.J., Wang, M. (2019). p21cip1/waf1 coordinate autophagy, proliferation and apoptosis in response to metabolic stress. Cancers 11 (8) : 1112. ScholarBank@NUS Repository. https://doi.org/10.3390/cancers11081112
Rights: Attribution 4.0 International
Abstract: Cancer cells possess metabolic properties that are different from benign cells. These unique characteristics have become attractive targets that are being actively investigated for cancer therapy. p21cip1/waf1, also known as Cyclin-Dependent Kinase inhibitor 1A, is encoded by the CDKN1A gene. It is a major p53 target gene involved in cell cycle progression that has been extensively evaluated. To date, p21 has been reported to regulate various cell functions, both dependent and independent of p53. Besides regulating the cell cycle, p21 also modulates apoptosis, induces senescence, and maintains cellular quiescence in response to various stimuli. p21 transcription is induced in response to stresses, including those from oxidative and chemotherapeutic treatment. A recent study has shown that in response to metabolic stresses such as nutrient and energy depletion, p21 expression is induced to regulate various cell functions. Despite the biological significance, the mechanism of p21 regulation in cancer adaptation to metabolic stress is underexplored and thus represents an exciting field. This review focuses on the recent development of p21 regulation in response to metabolic stress and its impact in inducing cell cycle arrest and death in cancer cells. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
Source Title: Cancers
URI: https://scholarbank.nus.edu.sg/handle/10635/209559
ISSN: 2072-6694
DOI: 10.3390/cancers11081112
Rights: Attribution 4.0 International
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