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Expert
Reviews in Molecular Medicine: http://www.expertreviews.org/
DOI: 10.1017/S1462399408000744; 1 July 2008
Abde
M. Abukhdeir and Ben Ho Park (2008) p21 and p27: roles in carcinogenesis and
drug resistance. Expert Rev. Mol. Med. Vol. 10, e19, DOI: 10.1017/S1462399408000744
p21 and p27: roles in carcinogenesis and drug resistance
Abde M. Abukhdeir a1
and Ben Ho Park a1 c1
a1 The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Breast Cancer Research Program, Baltimore, MD, USA.
c1 Corresponding author: Ben Ho Park, 1650 Orleans Street, CRBI, Room 1M42, Baltimore, MD 21231, USA. Tel: +1 410 502 7399; Fax: +1 410 614 8397; E-mail: bpark2@jhmi.edu
Human cancers arise from an imbalance of cell growth and cell death. Key proteins that govern this balance are those that mediate the cell cycle. Several different molecular effectors have been identified that tightly regulate specific phases of the cell cycle, including cyclins, cyclin-dependent kinases (CDKs) and CDK inhibitors. Notably, loss of expression or function of two G1-checkpoint CDK inhibitors – p21 (CDKN1A) and p27 (CDKN1B) – has been implicated in the genesis or progression of many human malignancies. Additionally, there is a growing body of evidence suggesting that functional loss of p21 or p27 can mediate a drug-resistance phenotype. However, reports in the literature have also suggested p21 and p27 can promote tumours, indicating a paradoxical effect. Here, we review historic and recent studies of these two CDK inhibitors, including their identification, function, importance to carcinogenesis and finally their roles in drug resistance.
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