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      GST gene polymorphisms and the risk of colorectal cancer development

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          Abstract

          Increasingly often, molecular studies of colorectal cancer focus on low penetrance genes. Among the factors potentially modifying the risk of contracting colorectal cancer is the glutathione S-transferase ( GST) gene family, encoding enzymes of the glutathione transferase type. Proteins of the GST family (glutathione S-transferases) are enzymes detoxifying a wide range of hazardous substances, such as reactive oxygen species (ROS) or xenobionts. Thus, their role, among other things, is the protection of DNA against oxidative damage, which may lead to mutations, and in consequence, favour carcinogenesis. GST gene polymorphisms may affect the functioning of the encoded enzymes, exerting an effect on the level of DNA damage, and therefore may have an indirect influence on the risk of the development of cancer. At present, there are many studies available concerning GST gene polymorphisms as factors modulating the risk of developing cancer, including colorectal cancer.

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          Red meat intake, doneness, polymorphisms in genes that encode carcinogen-metabolizing enzymes, and colorectal cancer risk.

          Richard C Boucher, Michelle Cotterchio, Johnathan Harper … (2008)
          Colorectal cancer literature regarding the interaction between polymorphisms in carcinogen-metabolizing enzymes and red meat intake/doneness is inconsistent. A case-control study was conducted to evaluate the interaction between red meat consumption, doneness, and polymorphisms in carcinogen-metabolizing enzymes. Colorectal cancer cases diagnosed 1997 to 2000, ages 20 to 74 years, were identified through the population-based Ontario Cancer Registry and recruited by the Ontario Family Colorectal Cancer Registry. Controls were sex-matched and age group-matched random sample of Ontario population. Epidemiologic and food questionnaires were completed by 1,095 cases and 1,890 controls; blood was provided by 842 and 1,251, respectively. Multivariate logistic regression was used to obtain adjusted odds ratio (OR) estimates. Increased red meat intake was associated with increased colorectal cancer risk [OR (> 5 versus 2 servings/wk well-done versus A variant significantly modified the association between red meat doneness intake and colorectal cancer risk. In conclusion, well-done red meat intake was associated with an increased risk of colorectal cancer regardless of carcinogen-metabolizing genotype, although our data suggest that persons with CYP1B1 and SULT1A1 variants had the highest colorectal cancer risk.
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            Polymorphisms in base excision repair genes as colorectal cancer risk factors and modifiers of the effect of diets high in red meat.

            Robert W. Haile, Loic Le Marchand, Ana Martinez … (2010)
            A diet high in red meat is an established colorectal cancer (CRC) risk factor. Carcinogens generated during meat cooking have been implicated as causal agents and can induce oxidative DNA damage, which elicits repair by the base excision repair (BER) pathway. Using a family-based study, we investigated the role of polymorphisms in 4 BER genes (APEX1 Gln51His, Asp148Glu; OGG1 Ser236Cys; PARP Val742Ala; and XRCC1 Arg194Trp, Arg280His, Arg399Gln) as potential CRC risk factors and modifiers of the association between diets high in red meat or poultry and CRC risk. We tested for gene-environment interactions using case-only analyses (n = 577) and compared statistically significant results with those obtained using case-unaffected sibling comparisons (n = 307 sibships). Carriers of the APEX1 codon 51 Gln/His genotype had a reduced CRC risk compared with carriers of the Gln/Gln genotype (odds ratio (OR) = 0.15, 95% CI = 0.03-0.69, P = 0.015). The association between higher red meat intake (>3 servings per week) and CRC was modified by the PARP Val762Ala single-nucleotide polymorphisms (SNP; case-only interaction P = 0.026). This SNP also modified the association between higher intake of high-temperature cooked red meat (case-only interaction P = 0.0009). We report evidence that the BER pathway PARP gene modifies the association of diets high in red meat cooked at high temperatures with risk of CRC. Our findings suggest a contribution to colorectal carcinogenesis of free radical damage as one of the possible harmful effects of a diet high in red meat. ©2010 AACR.
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              Glutathione S-transferase-micro1 regulates vascular smooth muscle cell proliferation, migration, and oxidative stress.

              Liqun Chi, Anh Le, David M. Malakauskas … (2009)
              Glutathione S-transferase-micro1, GSTM1, belongs to a superfamily of glutathione S-transferases that metabolizes a broad range of reactive oxygen species and xenobiotics. Across species, genetic variants that result in decreased expression of the Gstm1 gene are associated with increased susceptibility for vascular diseases, including atherosclerosis in humans. We previously identified Gstm1 as a positional candidate in our gene mapping study for susceptibility to renal vascular injury characterized by medial hypertrophy and hyperplasia of the renal vessels. To determine the role of Gstm1 in vascular smooth muscle cells (VSMCs), we isolated VSMCs from mouse aortas. We demonstrate that VSMCs from the susceptible C57BL/6 mice have reduced expression of Gstm1 mRNA and its protein product compared with that of the resistant 129 mice. After serum stimulation, C57BL/6 VSMCs proliferate and migrate at a much faster rate than 129 VSMCs. Furthermore, C57BL/6 VSMCs have higher levels of reactive oxygen species and exhibit exaggerated p38 mitogen-activated protein kinase phosphorylation after exposure to H(2)O(2). To establish causality, we show that knockdown of Gstm1 by small interfering RNA results in increased proliferation of VSMCs in a dose-dependent manner, as well as in increased reactive oxygen species levels and VSMC migration. Moreover, Gstm1 small interfering RNA causes increased p38 mitogen-activated protein kinase phosphorylation and attenuates the antiproliferative effect of Tempol. Our data suggest that Gstm1 is a novel regulator of VSMC proliferation and migration through its role in handling reactive oxygen species. Genetic variants that cause a decremental change in expression of Gstm1 may permit an environment of exaggerated oxidative stress, leading to susceptibility to vascular remodeling and atherosclerosis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Contemp Oncol (Pozn)
                Journal ID (iso-abbrev): Contemp Oncol (Pozn)
                Journal ID (publisher-id): WO
                Title: Contemporary Oncology
                Publisher: Termedia Publishing House
                ISSN (Print): 1428-2526
                ISSN (Electronic): 1897-4309
                Publication date (Electronic): 20 May 2014
                Publication date (Print): 2014
                Volume: 18
                Issue: 4
                Pages: 219-221
                Affiliations
                [1 ]Department of Surgery and Surgical Nursing, Institute of Nursing and Obstetrics, Faculty of Health Sciences, Jan Kochanowski University in Kielce, Kielce, Poland
                [2 ]Institute of Biology, Faculty of Mathematics and Natural Sciences, Jan Kochanowski University in Kielce, Kielce, Poland
                Author notes
                Address for correspondence: Justyna Klusek, Department of Surgery and Surgical Nursing, Institute of Nursing and Obstetrics, Faculty of Health Sciences, Jan Kochanowski University in Kielce, 25-317 Kielce. e-mail: justynaklusek@ 123456tlen.pl
                Article
                Publisher ID: 22437
                DOI: 10.5114/wo.2014.41388
                PMC ID: 4171468
                PubMed ID: 25258576
                SO-VID: 1295533d-55c7-4db0-a840-e8cfc096ad4e
                Copyright © Copyright © 2014 Termedia
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 November 2013
                Date revision received : 15 January 2014
                Date accepted : 26 February 2014
                Categories
                Subject: Review

                Keywords: tumours,colorectal cancer,glutathione transferases,gst genes
                Data availability:
                Keywords: tumours, colorectal cancer, glutathione transferases, gst genes

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