The accumulation of DNA repair defects is the molecular origin of carcinogenesis

被引:24
作者
Cha, Hyuk-Jin [1 ]
Yim, Hyungshin [2 ]
机构
[1] Sogang Univ, Dept Life Sci, Seoul 120742, South Korea
[2] Hanyang Univ, Coll Pharm, Inst Pharmaceut Sci & Technol, Dept Pharm, Ansan 426791, Kyeonggi Do, South Korea
基金
新加坡国家研究基金会;
关键词
Genomic instability; DNA damage; DNA repair; Cancer; Aging; STRAND BREAK REPAIR; DEPENDENT PROTEIN-KINASE; BASE EXCISION-REPAIR; DAMAGE RESPONSE; GENOMIC INSTABILITY; ATM ACTIVATION; ATAXIA-TELANGIECTASIA; CHECKPOINT ACTIVATION; MISMATCH-REPAIR; END RESECTION;
D O I
10.1007/s13277-013-1038-y
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Genomic instability has been considered to be one of the prominent factors for carcinogenesis and the development of a number of degenerative disorders, predominantly related to the aging. The cellular machineries involved in the maintenance of genomic integrity such as DNA repair and DNA damage responses are extensively characterized by a large number of studies. The failure of proper actions of such cellular machineries may lead to the devastating effects mostly inducing cancer or premature aging, even with no acute exogenous DNA damage stimuli. In this review, we especially focus on the pathophysiological aspects of the defective DNA damage responses in carcinogenesis and premature aging. Clear understanding the causes of carcinogenesis and age-related degenerative diseases will provide novel and efficient approaches for prevention and rational treatment of cancer and premature aging.
引用
收藏
页码:3293 / 3302
页数:10
相关论文
共 110 条
  • [1] BRCA1 expression restores radiation resistance in BRCA1-defective cancer cells through enhancement of transcription-coupled DNA repair
    Abbott, DW
    Thompson, ME
    Robinson-Benion, C
    Tomlinson, G
    Jensen, RA
    Holt, JT
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (26) : 18808 - 18812
  • [2] Cell cycle checkpoint signaling through the ATM and ATR kinases
    Abraham, RT
    [J]. GENES & DEVELOPMENT, 2001, 15 (17) : 2177 - 2196
  • [3] Enhanced phosphorylation of p53 by ATN in response to DNA damage
    Banin, S
    Moyal, L
    Shieh, SY
    Taya, Y
    Anderson, CW
    Chessa, L
    Smorodinsky, NI
    Prives, C
    Reiss, Y
    Shiloh, Y
    Ziv, Y
    [J]. SCIENCE, 1998, 281 (5383) : 1674 - 1677
  • [4] TOPping up ATR activity
    Bartek, J
    Mailand, N
    [J]. CELL, 2006, 124 (05) : 888 - 890
  • [5] Roles of ATM and NBS1 in chromatin structure modulation and DNA double-strand break repair
    Berkovich, Elijahu
    Monnat, Raymond J., Jr.
    Kastan, Michael B.
    [J]. NATURE CELL BIOLOGY, 2007, 9 (06) : 683 - U137
  • [6] Mismatch repair and response to DNA-damaging antitumour therapies
    Bignami, M
    Casorelli, I
    Karran, P
    [J]. EUROPEAN JOURNAL OF CANCER, 2003, 39 (15) : 2142 - 2149
  • [7] Structural basis for the methylation state-specific recognition of histone H4-K20 by 53BP1 and Crb2 in DNA repair
    Botuyan, Maria Victoria
    Lee, Joseph
    Ward, Irene M.
    Kim, Ja-Eun
    Thompson, James R.
    Chen, Junjie
    Mer, Georges
    [J]. CELL, 2006, 127 (07) : 1361 - 1373
  • [8] Functional uncoupling of MCM helicase and DNA polymerase activities activates the ATR-dependent checkpoint
    Byun, TS
    Pacek, M
    Yee, MC
    Walter, JC
    Cimprich, KA
    [J]. GENES & DEVELOPMENT, 2005, 19 (09) : 1040 - 1052
  • [9] Single-strand break repair and genetic disease
    Caldecott, Keith W.
    [J]. NATURE REVIEWS GENETICS, 2008, 9 (08) : 619 - 631
  • [10] Mammalian single-strand break repair: Mechanisms and links with chromatin
    Caldecott, Keith W.
    [J]. DNA REPAIR, 2007, 6 (04) : 443 - 453