Effect of gliclazide on nucleotide excision repair [NER] and non-homologous DNA end joining [NHEJ] in normal and cancer cells

• Autorzy: Sliwinska A. , Sliwinski T. , Kasznicki J. , Drzewoski J.
• Języki publikacji: EN

Abstrakty

EN

The results of clinical studies revealed that gliclazide may reduce the risk of cancer in type 2 diabetic patients (T2DM), although the mechanism of possible protective effect is not sufficiently explored. The increased level of DNA damage and impaired DNA repair system in diabetes mellitus may play a substantial role in neoplastic transformation. Recently, we have demonstrated that gliclazide protected DNA against damage introduced by the oxidative stress, but its action on the DNA repair mechanisms is unclear. Therefore, the aim of this study was to assess whether gliclazide has any effect on the DNA repair pathways, e.g. nucleotide excision repair (NER) and non-homologous end joining (NHEJ). NER activity was assessed in the extract of human lymphocytes and pancreatic cancer cells (PANC-1) treated or not with gliclazide by use of an UV-irradiated plasmid as a substrate and by quantitative PCR performed to evaluate the efficacy of the removal of UV-induced lesions from the p53 gene by intact cells. The efficacy of NHEJ pathway was examined by a simple and rapid in vitro assay based on fluorescent detection of repair products. We did not observe significant differences between the efficiency of NER and NHEJ for extracts of lymphocytes alone and lymphocytes treated with gliclazide. Contrary, gliclazide increased the efficacy of NER (46.0% vs. 84.0%, p<0.01) and NHEJ (58.0% vs. 66.0%, p<0.05) in PANC-1 cells. In conclusion, the present study showed that gliclazide did not affect NER and NHEJ in human normal cells, but it may stimulate DNA repair in cancer cells.

Słowa kluczowe

EN

gliclazide; nucleotide excisor repair; non-homologous and joining; diabetes; lymphocyte; pancreatic cancer cell; cancer cell; diabetes type 2; DNA damage; DNA repair; neoplastic transformation; oxidative stress

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2010
• Tom: 61
• Numer: 3
• Strony: 347-353
• Opis fizyczny: p.347-353,fig.,ref.

Twórcy

autor

Sliwinska A.

• Medical University of Lodz, Zgierz, Poland

autor

Sliwinski T.

autor

Kasznicki J.

autor

Drzewoski J.

Bibliografia

• Jennings PE, Scott NA, Saniabadi AR, Belch JJ. Effects of gliclazide on platelet reactivity and free radicals in type II diabetic patients: clinical assessment. Metabolism 1992; 41(Suppl. 1): 36-39.
• Monami M, Balzi D, Lamanna C, et al. Are sulphonylureas all the same? A cohort study on cardiovascular and cancer-related mortality. Diabetes Metab Res Rev 2007; 23: 479-484.
• Monami M, Lamanna C, Balzi D, Marchionni N, Mannucci E. Sulphonylureas and cancer: a case-control study. Acta Diabetol 2009; 46: 279-284.
• LeRoith D, Novosyadlyy R, Gallagher EJ, Lann D, Vijayakumar A, Yakar S. Obesity and type 2 diabetes are associated with an increased risk of developing cancer and a worse prognosis; epidemiological and mechanistic evidence. Exp Clin Endocrinol Diabetes 2008; 116(Suppl 1): S4-S6.
• Pan HZ, Chang D, Feng LG, Xu FJ, Kuang HY, Lu MJ. Oxidative damage to DNA and its relationship with diabetic complications. Biomed Environ Sci 2007; 20: 160-163.
• Goetz ME, Luch A. Reactive species: a cell damaging rout assisting to chemical carcinogens. Cancer Lett 2008; 18: 73-83.
• Dixon K, Kopras E. Genetic alterations and DNA repair in human carcinogenesis. Semin Cancer Biol 2004; 14: 441-448.
• Bjelland S, Seeberg E. Mutagenicity, toxicity and repair of DNA base damage induced by oxidation. Mutation Res 2003; 531: 37-80.
• Costa RM, Chigancas V, Galhardo Rda S, Carvalho H, Menck CF. The eukaryotic nucleotide excision repair pathway. Biochimie 2003; 85: 1083-1099.
• Caldecott KW. Single-strand break repair and genetic disease. Nat Rev Genet 2008; 9: 619-631.
• Yano K, Morotomi-Yano K, Adachi N, Akiyama H. Molecular mechanism of protein assembly on DNA double-strand breaks in the non-homologous end-joining pathway. J Radiat Res (Tokyo) 2009; 50: 97-108.
• Pardo B, Gomez-Gonzalez B, Aguilera A. DNA repair in mammalian cells: DNA double-strand break repair: how to fix a broken relationship. Cell Mol Life Sci 2009; 66: 1039-1056.
• Sliwinska A, Blasiak J, Drzewoski J. Effect of gliclazide on DNA damage in human peripheral blood lymphocytes and insulinoma mouse cells. Chem Biol Interact 2006; 162: 259-267.
• Sliwinska A, Blasiak J, Kasznicki J, Drzewoski J. in vitro effect of gliclazide on DNA damage and repair in patients with type 2 diabetes mellitus (T2DM). Chem Biol Interact 2008; 173: 159-165.
• Wood RD, Biggerstaff M, Shivji MKK. Detection and measurement of nucleotide excision repair synthesis by mammalian cell extracts in vitro. Methods 1995; 7: 163-175.
• Biggerstaff M, Robins P, Coverley D, Wood RD. Effect of exogenous DNA fragments on human cell extract-mediated DNA repair synthesis. Mutation Res 1991; 254: 217-224.
• Wood RD, Robins P, Lindahl T. Complementation of the xeroderma pigmentosum DNA repair defect in cell-free extracts. Cell 1988; 53: 97-106.
• Wang YC, Lee PJ, Shih CM, et al. Damage formation and repair efficiency in the p53 gene of cell lines and blood lymphocytes assayed by multiplex long quantitative polymerase chain reaction. Anal Biochem 2003; 319: 206-215.
• Bradford MM. A rapid and sensitive method for the quantification of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem 1976; 72: 248-254.
• Pastwa E, Poplawski T, Czechowska A, Malinowski M, Blasiak J. Non-homologous DNA end joining repair in normal and leukemic cells depends on the substrate ends. Z Naturforsch C 2005; 60: 493-500.
• Demkow U, Winklewski P, Potapinska O, Popko K, Lipinska A, Wasik M. The influence of insulin on calcium on concentration during transduction of signals into neutrophils. J Physiol Pharmacol 2008; 59(Suppl. 6): 219-229.
• Zayachkivaska O, Gzregotsky M, Ferentc M, Yaschenko A, Urbanovych A. Effects of nitrosative stress and reactive oxygen-scavenging systems in esophageal physiopathy under streptozotocin-induced experimental hyperglycemia. J Physiol Pharmacol 2008; 59(Suppl 2): 77-87.
• Sakowicz-Burkiewicz M, Kocbuch K, Grden M, Szutowicz A, Pawelczyk T. Protein kinase C mediated high glucose effect on adenosine receptors expression in rat B lymphocytes. J Physiol Pharmacol 2009; 60; 145-153.
• Altieri F, Grillo C, Maceroni M, Chichiarelli S. DNA damage and repair: from molecular mechanisms to health implications. Antioxid Redox Signal 2008; 10: 891-937.
• Shuck SC, Short EA, Turchi JJ. Eukaryotic nucleotide excision repair: from understanding mechanisms to influencing biology. Cell Res 2008; 18: 64-72.
• Maddukuri L, Dudzinska D, Tudek B. Bacterial DNA repair genes and their eukaryotic homologues: 4. The role of nucleotide excision DNA repair (NER) system in mammalian cells. Acta Biochim Pol 2007: 54: 469-482.
• Balajee AS, Bohr VA. Genomic heterogeneity of nucleotide excision repair. Gene 2000; 250: 15-30.
• Mahaney BL, Meek K, Lees-Miller SP Repair of ionizing radiation-induced DNA double-strand breaks by non-homologous end-joining. Biochem J 2009: 417: 639-650.
• Czornak K, Chughtai S, Chrzanowska KH. Mystery of DNA repair: the role of the MRN complex and ATM kinase in DNA damage repair. J Appl Genet 2008: 49: 383-396.
• Blasiak J, Arabski M, Krupa R, et al. DNA damage and repair in type 2 diabetes mellitus. Mutat Res 2004; 554: 297-304.
• Lieber M, Mazzetta J, Nelson-Rees W, Kaplan M, Todaro G. Establishment of a continuous tumor-cell line (PANC-1) from a human carcinoma of the exocrine pancreas. Int J Cancer 1975; 15: 741-747.
• Calabretta B, Kaczmarek L, Selleri L, et al. Growth-dependent expression of human Mr 53,000 tumor antigen messenger RNA in normal andneoplastic cells. Cancer Res 1986; 46: 5738-5742.
• Taghavi MH, Davoodi J. Restoration of p53 functions suppresses tumor growth of pancreatic cells with different p53 status. Cancer Biother Radiopharm 2007; 22: 322-332.
• Tang W, Willers H, Powell SN. p53 directly enhances rejoining of DNA double-strand breaks with cohesive ends in gamma-irradiated mouse fibroblasts. Cancer Res 1999; 59: 2562-2565.
• Yang T, Namba H, Hara T, et al. p53 induced by ionizing radiation mediates DNA end-jointing activity, but not apoptosis of thyroid cells. Oncogene 1997; 14: 1511-1519.
• Hill SM, Frasch T, Xiang S, Yuan L, Duplessis T, Mao L. Molecular mechanisms of melatonin anticancer effect. Integr Cancer Ther 2009; 8: 337-346.
• Leja-Szpak A, Jaworek J, Szklarczyk J, Konturek SJ, Pawlik WW. Melatonin stimulates HSP27 phosphorylation in human pancreatic carcinoma cells (PANC-1). J Physiol Pharmacol 2007; 58(Suppl. 3): 177-188.