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Int. J. Mol. Sci. 2014, 15(12), 22109-22127; doi:10.3390/ijms151222109

Battle Against Cancer: An Everlasting Saga of p53

1
School of Continuing Studies, Tulane University, New Orleans, LA 70118, USA
2
Department of Clinical Oncology, Queen Elizabeth Hospital, Hong Kong 999077, China
*
Authors to whom correspondence should be addressed.
Received: 20 September 2014 / Revised: 23 October 2014 / Accepted: 25 November 2014 / Published: 1 December 2014
(This article belongs to the Special Issue Advances in Molecular Oncology 2014)
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Abstract

Cancer is one of the most life-threatening diseases characterized by uncontrolled growth and spread of malignant cells. The tumor suppressor p53 is the master regulator of tumor cell growth and proliferation. In response to various stress signals, p53 can be activated and transcriptionally induces a myriad of target genes, including both protein-encoding and non-coding genes, controlling cell cycle progression, DNA repair, senescence, apoptosis, autophagy and metabolism of tumor cells. However, around 50% of human cancers harbor mutant p53 and, in the majority of the remaining cancers, p53 is inactivated through multiple mechanisms. Herein, we review the recent progress in understanding the molecular basis of p53 signaling, particularly the newly identified ribosomal stress—p53 pathway, and the development of chemotherapeutics via activating wild-type p53 or restoring mutant p53 functions in cancer. A full understanding of p53 regulation will aid the development of effective cancer treatments. View Full-Text
Keywords: p53; mutant p53; MDM2; ribosomal stress; transcription; cancer chemotherapeutics p53; mutant p53; MDM2; ribosomal stress; transcription; cancer chemotherapeutics
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Hao, Q.; Cho, W.C. Battle Against Cancer: An Everlasting Saga of p53. Int. J. Mol. Sci. 2014, 15, 22109-22127.

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