p53, autophagy and tumor suppression

被引:71
作者
Jin, SK [1 ]
机构
[1] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pharmacol, Piscataway, NJ 08854 USA
[2] Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Canc Inst New Jersey, Piscataway, NJ 08854 USA
关键词
p53; autophagy; tumor suppression; beclin; 1; mTOR; apoptosis; necrosis;
D O I
10.4161/auto.1.3.2051
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Autophagy was recently established as a novel tumor suppression mechanism, which stimulated a wave of investigations that were aimed at understanding exactly how autophagy prevents tumorigenesis, as well as to determine to what extent autophogy is implicated in human cancers. Autophagy might exert its tumor suppression function at the subcellular level by removing defective cytoplasmic components, such as damaged mitochondria. In addition, it might function at the cellular level by helping in the orderly removal of damaged cells. Previous studies indicated that autophagy is compromised in human breast, ovarian and prostate cancers. Recent research revealed that autophogy is activated by p53, a critical tumor suppressor that is involved in most, if not all, tumorigenesis. This study places autophagy in a broader context of human cancers. Future work elucidating the role of autophagy in the p53 circuit and p53 function might provide more insight into tumorigenesis and targeted cancer chemotherapy.
引用
收藏
页码:171 / 173
页数:3
相关论文
共 32 条
  • [1] Cloning and genomic organization of beclin 1, a candidate tumor suppressor gene on chromosome 17q21
    Aita, VM
    Liang, XH
    Murty, VVVS
    Pincus, DL
    Yu, WP
    Cayanis, E
    Kalachikov, S
    Gilliam, TC
    Levine, B
    [J]. GENOMICS, 1999, 59 (01) : 59 - 65
  • [2] Balsara BR, 2001, GENE CHROMOSOME CANC, V30, P245, DOI 10.1002/1098-2264(2000)9999:9999<::AID-GCC1083>3.0.CO
  • [3] 2-M
  • [4] Bando K, 2000, GENE CHROMOSOME CANC, V28, P38, DOI 10.1002/(SICI)1098-2264(200005)28:1<38::AID-GCC5>3.0.CO
  • [5] 2-A
  • [6] New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase AKT pathway
    Cantley, LC
    Neel, BG
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (08) : 4240 - 4245
  • [7] Chen TP, 1996, CANCER RES, V56, P5605
  • [8] Elo JP, 1997, CANCER RES, V57, P3356
  • [9] The coordinate regulation of the p53 and rnTOR pathways in cells
    Feng, ZH
    Zhang, H
    Levine, AJ
    Jin, S
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2005, 102 (23) : 8204 - 8209
  • [10] Regulation of translation initiation by FRAP/mTOR
    Gingras, AC
    Raught, B
    Sonenberg, N
    [J]. GENES & DEVELOPMENT, 2001, 15 (07) : 807 - 826