Evidence for base excision repair processing of DNA interstrand crosslinks

被引:19
作者
Kothandapani, Anbarasi [1 ]
Patrick, Steve M. [1 ]
机构
[1] Univ Toledo, Dept Biochem & Canc Biol, Toledo, OH 43614 USA
基金
美国国家卫生研究院;
关键词
AP endonuclease; Base excision repair; BCNU; Cisplatin; DNA glycosylase; Interstrand crosslinks; Mitomycin C; Nitrogen mustard; Oxaliplatin; Psoralen; DNA Polymerase beta; APURINIC/APYRIMIDINIC ENDONUCLEASE ACTIVITY; ENHANCES CELLULAR-SENSITIVITY; CANCER-ASSOCIATED VARIANTS; SMALL-MOLECULE INHIBITORS; LONG-PATCH REPAIR; POLYMERASE-BETA; HOMOLOGOUS RECOMBINATION; CISPLATIN CYTOTOXICITY; APHIDICOLIN GLYCINATE; THERAPEUTIC TARGETS;
D O I
10.1016/j.mrfmmm.2012.11.007
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Many bifunctional alkylating agents and anticancer drugs exert their cytotoxicity by producing cross links between the two complementary strands of DNA, termed interstrand crosslinks (ICLs). This blocks the strand separating processes during DNA replication and transcription, which can lead to cell cycle arrest and apoptosis. Cells use multiple DNA repair systems to eliminate the ICLs. Concerted action of repair proteins involved in Nucleotide Excision Repair and Homologous Recombination pathways are suggested to play a key role in the ICL repair. However, recent studies indicate a possible role for Base Excision Repair (BER) in mediating the cytotoxicity of ICL inducing agents in mammalian cells. Elucidating the mechanism of BER mediated modulation of ICL repair would help in understanding the recognition and removal of ICLs and aid in the development of potential therapeutic agents. In this review, the influence of BER proteins on ICL DNA repair and the possible mechanisms of action are discussed. (C) 2012 Elsevier B.V. All rights reserved.
引用
收藏
页码:44 / 52
页数:9
相关论文
共 157 条
[21]   Psoralen-induced DNA adducts are substrates for the base excision repair pathway in human cells [J].
Couve-Privat, Sophie ;
Mace, Gaetane ;
Rosselli, Filippo ;
Saparbaev, Murat K. .
NUCLEIC ACIDS RESEARCH, 2007, 35 (17) :5672-5682
[22]   ACTIVITY OF APHIDICOLIN GLYCINATE ALONE OR IN COMBINATION WITH CISPLATIN IN A MURINE OVARIAN TUMOR RESISTANT TO CISPLATIN [J].
DAMIA, G ;
TAGLIABUE, G ;
ZUCCHETTI, M ;
DAVOLI, E ;
SESSA, C ;
CAVALLI, F ;
DINCALCI, M .
CANCER CHEMOTHERAPY AND PHARMACOLOGY, 1992, 30 (06) :459-464
[23]   Mechanisms of resistance to alkylating agents [J].
Damia, G ;
D'Incalci, M .
CYTOTECHNOLOGY, 1998, 27 (1-3) :165-173
[24]   Translesion replication by DNA polymerase δ depends on processivity accessory proteins and differs in specificity from DNA polymerase β [J].
Daube, SS ;
Tomer, G ;
Livneh, Z .
BIOCHEMISTRY, 2000, 39 (02) :348-355
[25]   Base-excision repair of oxidative DNA damage [J].
David, Sheila S. ;
O'Shea, Valerie L. ;
Kundu, Sucharita .
NATURE, 2007, 447 (7147) :941-950
[26]  
Dogliotti E, 2001, PROG NUCLEIC ACID RE, V68, P3
[27]   Repair of DNA interstrand cross-links [J].
Dronkert, MLG ;
Kanaar, R .
MUTATION RESEARCH-DNA REPAIR, 2001, 486 (04) :217-247
[28]   Repair-deficient 3-methyladenine DNA glycosylase homozygous mutant mouse cells have increased sensitivity to alkylation-induced chromosome damage and cell killing [J].
Engelward, BP ;
Dreslin, A ;
Christensen, J ;
Huszar, D ;
Kurahara, C ;
Samson, L .
EMBO JOURNAL, 1996, 15 (04) :945-952
[29]   An NMR study of [d(CGCGAATTCGCG)](2) containing an interstrand cross-link derived from a distamycin-pyrrole conjugate [J].
Fagan, PA ;
Spielmann, HP ;
Sigurdsson, ST ;
Rink, SM ;
Hopkins, PB ;
Wemmer, DE .
NUCLEIC ACIDS RESEARCH, 1996, 24 (08) :1566-1573
[30]   Inhibition of Poly(ADP-Ribose) Polymerase in Tumors from BRCA Mutation Carriers. [J].
Fong, Peter C. ;
Boss, David S. ;
Yap, Timothy A. ;
Tutt, Andrew ;
Wu, Peijun ;
Mergui-Roelvink, Marja ;
Mortimer, Peter ;
Swaisland, Helen ;
Lau, Alan ;
O'Connor, Mark J. ;
Ashworth, Alan ;
Carmichael, James ;
Kaye, Stan B. ;
Schellens, Jan H. M. ;
de Bono, Johann S. .
NEW ENGLAND JOURNAL OF MEDICINE, 2009, 361 (02) :123-134