Yıl: 2007 Cilt: 32 Sayı: 3 Sayfa Aralığı: 104 - 111 Metin Dili: Türkçe İndeks Tarihi: 29-07-2022

Nükleotid eksizyon onarımı ve kanser

Öz:
Genomik DNA’da çevresel etmenlerle veya kendiliğinden oluşan DNA hasarları ya çeşitli DNA onarım mekanizmaları ile onarılır veya hücrenin programlı ölümüne neden olur. Canlı organizmalarda direkt DNA onarımı, nükleotid ve baz eksizyon onarımı, rekombinasyonel onarım gibi çeşitli DNA onarım mekanizmaları tanımlanmıştır. Bu mekanizmalar arasında nükleotid eksizyon onarımı bilinen en genel ve etkili onarım mekanizmasıdır. Nükleotid eksizyon onarım mekanizmasının yeterince işlev görememesi yaşlanma, kanser oluşumu, çeşitli kalıtsal ve nörodejeneratif bozukluklar ile sonuçlanır. Nükleotid eksizyon onarım mekanizmasının bozuk olduğu genetik geçişli nadir görülen üç sendrom tanımlanmıştır: Kseroderma pigmentosum, Cockayne sendromu, trikotiyodistrofi. Bunlardan kseroderma pigmentozumda deri ve iç organ kanserleri sıklığında artış, bazı olgularda nörolojik bulgular görülmesi dikkat çekicidir. Kanserin moleküler mekanizmalarının anlaşılması ve yeni tedavi stratejilerinin belirlenmesinde bu sendromlar önemlidir. Klinik araştırmalarda sağlıklı kişilerde nükleotid eksizyon onarımı kapasitesindeki çeşitliliklerin çeşitli kanser türlerine yatkınlıkta etkili olduğu düşünülmektedir. Artmış DNA onarımının ayrıca cerrahi olmayan kanser tedavilerinde tedaviye direnç gelişiminde önemli bir faktör olabileceği saptanmıştır.
Anahtar Kelime:

Konular: Biyokimya ve Moleküler Biyoloji

Nucleotide excision repair and cancer

Öz:
Enviromental or endogenous DNA damages of genomic DNA are either repaired by DNA repair mechanisms or lead apoptosis in living organisms. There are different DNA repair mechanisms such as direct DNA repair, nucleotide and base excision repair, recombinational repair. The most general and efficient repair mechanism known in living organisms is nucleotide excision repair pathway. Defects in nucleotide excision repair results in aging, carcinogenesis, various genetic and neurodegenerative disorders. Xeroderma pigmentosum, Cockayne syndrome and tricothiodystrophy are three rare hereditary disorders with nucleotide excision repair deficiency. Xeroderma pigmentosum is characterized with increased frequency of skin and internal organ cancers and in some case neurological abnormalities. These syndromes are very important to understand the molecular mechanisms of cancer and to design new therapeutic strategies. In normal population, interindividual variations in nucleotide excision repair capacity might be correlated with cancer proneness. Increased DNA repair capacity is also implicated in resistance of nonchirurgical cancer treatments.
Anahtar Kelime:

Konular: Biyokimya ve Moleküler Biyoloji
Belge Türü: Makale Makale Türü: Derleme Erişim Türü: Erişime Açık
  • [1] Orren DK, Sancar A. [1987]New discoveries in the enzymology of DNA repair. Cancer Rev 7: 5-27.
  • [2] Sancar A, Lindsey-Boltz LA, Ünsal-Kaçmaz K, Linn S. Molecular mechanisms of Mammalian DNA repair and the DNA damage checkpoints. [2004]Annu Rev Biochem. 73: 39-85.
  • [3] Friedberg EC. [1984]DNA Repair, s:1-2. Freeman WH and Company, New York.
  • [4] de Baer J, Hoeijmakers JHJ. [2000]Nucleotide excision repair and human syndromes. Carcinogenesis. 21 [3]: 453-460.
  • [5] Cooper GM [2000]The Cell, A Molecular Approach, s: 192-199, ASM press, Washington D.C.
  • [6] Sancar A. [1984]Mechanisms of DNA excision repair. Science 266 [23]: 1954-1956.
  • [7] Huang JC, Svobada DL, Reardon JT, Sancar A. [1992]Human nucleotide excision nuclease removes thymine dimers from DNA by incising the 22nd phoshodiester bond 5´ and the 6th phosphodiester bond 3’ to the photodimer. Proc Natl Acad Sci USA. 89: 3664-3668.
  • [8] Friedberg EC, Walker GC, Siede W. [1995]DNA Repair and Mutagenesis. s: 24-25, ASM press, Washington DC.
  • [9] Sancar A. [1996]DNA excision repair. Annu Rev Biochem. 65: 43-81.
  • [10] Petit C, Sancar A. [1999]Nucleotide excision repair: From E. Coli to man. Biochimie. 81: 15-25.
  • [11] Sancar A, Reardon JT. [2004]Nucleotide excision repair in E.Coli and Man. Advances in Protein Chemistry. 69: 43-71.
  • [12] Reardon JT, Bessho T, Kung HC, Balton PH, Sancar A. [1997]In vitro repair of oxidative DNA damage by human nucleotide excision repair system:possible explanation for neurodegeneration in xeroderma pigmentosum patients Proc Nat Acad Sci USA. 94: 9463-9468.
  • [13] Sancar A, Rupp WD. [1983]A novel repair enzyme: Uvr ABC excision nuclease of Esherishia Coli cuts a DNA strand on both sides of the damaged region Cell. 33: 249-260.
  • [14] Öğrünç M, Becker DF, Ragsdale SW, Sancar A. [1998]Nucleotide excision repair: from E. Coli to man. Biochimie. 81: 15-25.
  • [15] Reardon JT, Nichols AF, Keeney S, Smith CA, Taylor JS, Linn S, Sancar A. [1993]Comparative analysis of binding of human damaged DNA binding protein [XPE]and Esherishia Coli damage recognition protein [UvrA]to the major ultraviolet photoproducts: T[c,s]T, T[t,s]T, T[6-4T]T, and T[Dewar]T. J Biol Chem. 5, 268 [28]: 21301-21308.
  • [16] Tang, J, Chu G. [2002]Xeroderma pigmentosum group E and UV-damaged DNA binding protein. DNA Repair 1: 601-616.
  • [17] Tang JY, Hwang BJ, Ford JM, Hanawalt PC. [2000]Xeroderma pigmentosum p48 gene enhances global genomic repair and suppress UV-induced mutagenesis. Mol Cell. 5[4]: 737-744.
  • [18] Wakasugi M, Kawashima A, Morioka H, Linn S, Sancar A ve ark. [2002]DDB accumulates at DNA damage sites immediately after UV irradiation and directly stimulates nucleotide excision repair. J Biol Chem. 277[3]: 1637-1640.
  • [19] Kulaksiz G, Reardon JT, Sancar A. [2005]. Xeroderma pigmentosum complementation group E protein [XPE/DDB2]: purification of various complexes of XPE and analyses of their damaged DNA binding and putative DNA repair properties. Mol Cell Biol 25 [22]: 9784-92.
  • [20] Kulaksız G [Tez Danışmanları: Prof. Dr. Nazmi Özer, Prof. Dr. Aziz Sancar][2006]. Kseroderma Pigmentozum Grup E Proteini ve Komplekslerinin Saflaştırılması ve Nükleotid Eksizyon Tamir Mekanizmasındaki İşlevlerinin Belirlenmesi. Hacettepe Üniversitesi Sağlık Bilimleri Enstitüsü Doktora Tezi, Ankara.
  • [21] Branum ME, Reardon JT, Sancar A. [2001]DNA repair excision nuclease attacks undamaged DNA. A potential source of spontaneous mutations. J Biol Chem. 276 [27]: 25421-25426.
  • [22] Bohr VA, Smith CA, Okumoto DS, Hanawalt PC. [1985]DNA repair in an active gene: removal of pyrimidine dimers from the DHFR gene of CHO cells is much more efficient than in the genome overall. Cell, 40 [2]: 359-369.
  • [23] Venema J, Mullenders LHF, Natarajan AT, van Zeeland AA, Mullenders LH. [1990]The residual repair capacity of xeroderma pigmentosum complementation group C fibroblasts is highly specific for transcriptionally active DNA. Nucleic Acids Res. 18: 443-448.
  • [24] Friedberg EC [1996]Relationships between DNA repair and transcription. Annu Rev Biochem. 65: 15-42.
  • [25] van Gool AJ, Citterio E, Rodemakers J, van Os R, Vermeulen W, Constantiu A, Egly JM, Bootsma D, Hoeijmakers JH. [1997]The Cockayne syndrome B protein, involved in transcription coupled DNA repair, resides in an RNA polymerase II.containing complex. EMBO J. 16 [19]: 5655-5665.
  • [26] Hanawalt PC. [2002]Subpathways of nucleotide excision rapair and their regulation. Oncogene. 21: 8949-8956.
  • [27] de Boer J, Hoeijmakers JHJ, Cleaver JE ve Kraemer KH. [2001]The Metabolic Basis of Inherited Diseases. [Eds. Scriver, C.R., Beaudet, A.L., Sly, W.S. ve Valler, D.]Vol: 3, 28, 690-692 Mc Graw Hill, New York.
  • [28] Boyer JC, Kauffmann WK, Brylawsky BP, Cordeiro Stone M. [1990]Defective postreplication repair in xeroderma pigmentosum variant fibroblasts. Cancer Res. 50: 2593-2598.
  • [29] Rockx DAP, Mason R, van Hoffen A, Barton MC, Citterio E, Bregman DB, van Zeeland AA, Vrieling H & Mullenders LHF. [2000]UV-induced inhibition of transcription involves repression of transcription initiation and phosphorylation of RNA polymerase II. Proc Natl Acad Sci USA. 97: 10503–10508.
  • [30] Ljungman M, Zhang F [1996]Blockage of RNA polymerase as a possible trigger for UV-light induced apoptosis. Oncogene. 30: 823-831.
  • [31] Berg RJ, Rebel H, van der Horst GT, van Kranen HJ, Mullenders LH, van Vloten WA, de Gruijl FR. [2000]Impact of global genome repair versus transcription-coupled repair on ultraviolet carcinogenesis in hairless mice. Cancer Res. 60 [11]: 2858-63.
  • [32] Parris CN, Kraemer KH. [1993]Ultraviolet-induced mutations in Cockayne syndrome cells are primarily caused by cyclobutane dimer photoproducts while repair of other photoproducts is normal. Proc Natl Acad Sci USA. 90 [15]: 7260-4.
  • [33] Itin P H, Sarasin A, Pittelkow M R. [2001]Trichothiodystrophy: update on the sulfur-deficient brittle hair syndromes. J Am Acad Dermatol. 44: 891–920.
  • [34] Quilliet X, Chevallier-Lapente O, Zeng L, Calvayrac R, Mezzina M, Sarasin A, Vuillaume M. [1997]Retroviral-mediated correction of DNA repair defect in xeroderma pigmentosum cells in associated with recovery of catalase activity. Mutat Res. 385: 235-242.
  • [35] Nickoloff JA, Hoekstra MF. [1998]DNA Damage and Repair’de Nucleotide Excision Repair, Its relation to Human Disease [Derleyen Thompson LH]2. cilt, s:Kraemer KH, Patronas NJ, Shiffmann R, Brooks BP, Tamura D, Digiovanna JJ. [2007]Xeroderma pigmentosum, trichothiyodistrophy and Cockayne syndrome. A complex phenotype-genotype relationship. Neuroscience. 145: 1388-1396.
  • [36] Kraemer KH. [1997]Sunlight and skin cancer: another link revealed. Proc Natl Acad Sci USA. 94:11–4.
  • [37] Giglia-Mari G, Coin F, Ranish JA, Hoogstraten D, Theil A, Wijgers N, Jaspers NG, Raams A, Argentini M, Van Der Spek MPJ, Botta E, Stefanini M, Egly JM, Aebersold R, Hoeijmakers JH, Vermeulen W. [2004]A new, tenth subunit of TFIIH is responsible for the DNA repair syndrome trichothiodystrophy group A. Nat Genet. 36: 714–719.
  • [38] Mc Whir J, Selfridge J, Harrison DJ, Squires S, Melton DW. [1993]Mice with DNA repair gene [ERCC1]deficiency have elevated level of p53, liver nuclear abnormalities and die before weaning. Nat Genet. 5[3]: 207-208.
  • [39] Weeda G, Donker I, de Wit J, Morreau H, Jannsens R, Vissers CJ, Nigg A, van Steeg H, Bootsma D, Hoeijmakers JH. [1997]Disruption of mouse ERCC1 results in a novel repair syndrome with growth failure, nuclear abnormalities and senescence. Curr Biol. 7[6]: 427-439.
  • [40] Nakane H, Takeuchi S, Yuba S, Saijo M, Nakatsu Y, Murai H, Nakatsuru Y, Ishikawa T, Hirota S, Kitamura Y, Kato Y, Tsunoda Y, Miyauchi H, Horio T, Tokunaga T, Matsunaga T, Nikaido O, Nishimune Y, Okada Y, Tanaka K. [1995]High incidence of ultraviolet-B-or chemical-carcinogen-induced skin tumours in mice lacking the xeroderma pigmentosum groupA gene. Nature. 377: 165–168.
  • [41] de Vries A, van Oostrom CTh, Dortant PM, Beems RB, van Kreijl CB, Capel PJ, van Steeg H. [1997]Spontaneous liver tumors and benzo[a]pyrene-induced lymphomas in XPAdeficient mice. Mol Carcinog. 19: 46–53.
  • [42] Sands AT, Abuin A, Sanchez A, Conti CJ, Bradley A [1995]High susceptibility to ultraviolet-induced carcinogenesis in mice lacking XPC. Nature. 377: 162–165.
  • [43] Hollander MC, Philburn RT, Patterson AD, Velasco-Miguel S, Friedberg EC, Linnoila RI, Fornace Jr AR. [2005]Deletion of XPC leads to lung tumors in mice and is associated with early events in human lung carcinogenesis. Proc Natl Acad Sci USA. 102: 13200–13205.
  • [44] Yoon, T., Chakrabortty, A., Franks, R., Vali, T., Kiyokawa, H., Rachaudri, P., Tumor-prone phenotype of the DDB2-deficient mice, Oncogene. 24[3], 469-478, 2005.
  • [45] Wijnhoven SW, Hoogervorst EM, de Waard H, van der Horst GT, van Steeg H. [2007]Tissue specific mutagenic and carcinogenic
APA KULAKSIZ ERKMEN G, SANCAR A (2007). Nükleotid eksizyon onarımı ve kanser. , 104 - 111.
Chicago KULAKSIZ ERKMEN GÜLNİHAL,SANCAR Aziz Nükleotid eksizyon onarımı ve kanser. (2007): 104 - 111.
MLA KULAKSIZ ERKMEN GÜLNİHAL,SANCAR Aziz Nükleotid eksizyon onarımı ve kanser. , 2007, ss.104 - 111.
AMA KULAKSIZ ERKMEN G,SANCAR A Nükleotid eksizyon onarımı ve kanser. . 2007; 104 - 111.
Vancouver KULAKSIZ ERKMEN G,SANCAR A Nükleotid eksizyon onarımı ve kanser. . 2007; 104 - 111.
IEEE KULAKSIZ ERKMEN G,SANCAR A "Nükleotid eksizyon onarımı ve kanser." , ss.104 - 111, 2007.
ISNAD KULAKSIZ ERKMEN, GÜLNİHAL - SANCAR, Aziz. "Nükleotid eksizyon onarımı ve kanser". (2007), 104-111.
APA KULAKSIZ ERKMEN G, SANCAR A (2007). Nükleotid eksizyon onarımı ve kanser. Türk Biyokimya Dergisi, 32(3), 104 - 111.
Chicago KULAKSIZ ERKMEN GÜLNİHAL,SANCAR Aziz Nükleotid eksizyon onarımı ve kanser. Türk Biyokimya Dergisi 32, no.3 (2007): 104 - 111.
MLA KULAKSIZ ERKMEN GÜLNİHAL,SANCAR Aziz Nükleotid eksizyon onarımı ve kanser. Türk Biyokimya Dergisi, vol.32, no.3, 2007, ss.104 - 111.
AMA KULAKSIZ ERKMEN G,SANCAR A Nükleotid eksizyon onarımı ve kanser. Türk Biyokimya Dergisi. 2007; 32(3): 104 - 111.
Vancouver KULAKSIZ ERKMEN G,SANCAR A Nükleotid eksizyon onarımı ve kanser. Türk Biyokimya Dergisi. 2007; 32(3): 104 - 111.
IEEE KULAKSIZ ERKMEN G,SANCAR A "Nükleotid eksizyon onarımı ve kanser." Türk Biyokimya Dergisi, 32, ss.104 - 111, 2007.
ISNAD KULAKSIZ ERKMEN, GÜLNİHAL - SANCAR, Aziz. "Nükleotid eksizyon onarımı ve kanser". Türk Biyokimya Dergisi 32/3 (2007), 104-111.