p21Waf1/Cip1: its paradoxical effect in the regulation of breast cancer View Full Text


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Article Info

DATE

2019-03

AUTHORS

Samir F. Zohny, Abdulrahman L. Al-Malki, Mazin A. Zamzami, Hani Choudhry

ABSTRACT

p21Waf1/Cip1, the cyclin-dependent kinase (CDK) inhibitor belonging to the KIP/CIP family, was initially regarded as a tumor suppressor protein because it was recognized as the chief mediator of p53-dependent cell cycle arrest elicited by DNA damage. Conversely, it has been proposed that p21Waf1/Cip1 may also function as an oncogene because it can inhibit apoptosis. Thus, p21Waf1/Cip1 is regarded as a protein with a dual behavior, as its expression might cause potential benefits or dangerous effects in breast cancer. Consequently, careful planning is required in targeting p21Waf1/Cip1 expression for therapy of breast cancer patients. This review illustrates the discovery and mechanisms of induction of p21Waf1/Cip1. Then, we focus on elucidating the paradoxical effect of p21Waf1/Cip1 expression on human breast carcinogenesis and explaining how the subcellular localization (nuclear or cytoplasmic) of p21Waf1/Cip1 has an impact on both determining its fate as either cell-growth inhibitor or antiapoptotic molecule and, its effect on clinicopathological factors and prognosis of breast cancer patients. Moreover, we explore how the pattern of the p21Waf1/Cip1 could affect the responsiveness of human breast cancer to chemotherapy. Furthermore, the pharmacological approaches to target p21Waf1/Cip1 expression for therapy of breast cancer are clarified. More... »

PAGES

131-137

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12282-018-0913-1

DOI

http://dx.doi.org/10.1007/s12282-018-0913-1

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30255294


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46 schema:description p21<sup>Waf1/Cip1</sup>, the cyclin-dependent kinase (CDK) inhibitor belonging to the KIP/CIP family, was initially regarded as a tumor suppressor protein because it was recognized as the chief mediator of p53-dependent cell cycle arrest elicited by DNA damage. Conversely, it has been proposed that p21<sup>Waf1/Cip1</sup> may also function as an oncogene because it can inhibit apoptosis. Thus, p21<sup>Waf1/Cip1</sup> is regarded as a protein with a dual behavior, as its expression might cause potential benefits or dangerous effects in breast cancer. Consequently, careful planning is required in targeting p21<sup>Waf1/Cip1</sup> expression for therapy of breast cancer patients. This review illustrates the discovery and mechanisms of induction of p21<sup>Waf1/Cip1</sup>. Then, we focus on elucidating the paradoxical effect of p21<sup>Waf1/Cip1</sup> expression on human breast carcinogenesis and explaining how the subcellular localization (nuclear or cytoplasmic) of p21<sup>Waf1/Cip1</sup> has an impact on both determining its fate as either cell-growth inhibitor or antiapoptotic molecule and, its effect on clinicopathological factors and prognosis of breast cancer patients. Moreover, we explore how the pattern of the p21<sup>Waf1/Cip1</sup> could affect the responsiveness of human breast cancer to chemotherapy. Furthermore, the pharmacological approaches to target p21<sup>Waf1/Cip1</sup> expression for therapy of breast cancer are clarified.
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