p53 as an intervention target for cancer and aging

被引:46
作者
Hasty, Paul [1 ,2 ,3 ]
Christy, Barbara A. [1 ]
机构
[1] Univ Texas Hlth Sci Ctr San Antonio, Inst Biotechnol, Dept Mol Med, San Antonio, TX 78245 USA
[2] Univ Texas Hlth Sci Ctr San Antonio, Canc Therapy & Res Ctr, San Antonio, TX 78245 USA
[3] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst Longev & Aging Studies, San Antonio, TX 78245 USA
来源
PATHOBIOLOGY OF AGING AND AGE-RELATED DISEASES | 2013年 / 3卷 / 01期
关键词
DNA damage; cell growth; cellular senescence; apoptosis; anaerobic glycolysis;
D O I
10.3402/pba.v3i0.22702
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
p53 is well known for suppressing tumors but could also affect other aging processes not associated with tumor suppression. As a transcription factor, p53 responds to a variety of stresses to either induce apoptosis (cell death) or cell cycle arrest (cell preservation) to suppress tumor development. Yet, the effect p53 has on the non-cancer aspects of aging is complicated and not well understood. On one side, p53 could induce cellular senescence or apoptosis to suppress cancer but as an unintended consequence enhance the aging process especially if these responses diminish stem and progenitor cell populations. But on the flip side, p53 could reduce growth and growth-related stress to enable cell survival and ultimately delay the aging process. A better understanding of diverse functions of p53 is essential to elucidate its influences on the aging process and the possibility of targeting p53 or p53 transcriptional targets to treat cancer and ameliorate general aging.
引用
收藏
页数:11
相关论文
共 135 条
  • [91] Heterodimerization of Mdm2 and Mdm4 is critical for regulating p53 activity during embryogenesis but dispensable for p53 and Mdm2 stability
    Pant, Vinod
    Xiong, Shunbin
    Iwakuma, Tomoo
    Quintas-Cardama, Alfonso
    Lozano, Guillermina
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2011, 108 (29) : 11995 - 12000
  • [92] Rescue of embryonic lethality in Mdm4-null mice by loss of Trp53 suggests a nonoverlapping pathway with MDM2 to regulate p53
    Parant, J
    Chavez-Reyes, A
    Little, NA
    Yan, W
    Reinke, V
    Jochemsen, AG
    Lozano, G
    [J]. NATURE GENETICS, 2001, 29 (01) : 92 - 95
  • [93] Activation of AMP-Activated Protein Kinase Inhibits the Proliferation of Human Endothelial Cells
    Peyton, Kelly J.
    Liu, Xiao-ming
    Yu, Yajie
    Yates, Benjamin
    Durante, William
    [J]. JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2012, 342 (03) : 827 - 834
  • [94] Pseudo-NORs: A novel model for studying nucleoli
    Prieto, Jose-Luis
    McStay, Brian
    [J]. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 2008, 1783 (11): : 2116 - 2123
  • [95] Stress and mTORture signaling
    Reiling, J. H.
    Sabatini, D. M.
    [J]. ONCOGENE, 2006, 25 (48) : 6373 - 6383
  • [96] A novel human p53 isoform is an essential element of the ATR-intra-S phase checkpoint
    Rohaly, G
    Chemnitz, J
    Dehde, S
    Nunez, AM
    Heukeshoven, J
    Deppert, W
    Dornreiter, I
    [J]. CELL, 2005, 122 (01) : 21 - 32
  • [97] p53 Guardian of a Genome's Guardian?
    Rubbi, Carlos P.
    Milner, Jo
    [J]. CELL CYCLE, 2003, 2 (01) : 18 - 19
  • [98] Disruption of the nucleolus mediates stabilization of p53 in response to DNA damage and other stresses
    Rubbi, CP
    Milner, J
    [J]. EMBO JOURNAL, 2003, 22 (22) : 6068 - 6077
  • [99] A SUBSET OF P53-DEFICIENT EMBRYOS EXHIBIT EXENCEPHALY
    SAH, VP
    ATTARDI, LD
    MULLIGAN, GJ
    WILLIAMS, BO
    BRONSON, RT
    JACKS, T
    [J]. NATURE GENETICS, 1995, 10 (02) : 175 - 180
  • [100] Specific Activation of mTORC1 by Rheb G-protein in Vitro Involves Enhanced Recruitment of Its Substrate Protein
    Sato, Tatsuhiro
    Nakashima, Akio
    Guo, Lea
    Tamanoi, Fuyuhiko
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2009, 284 (19) : 12783 - 12791