M. A. Rosales-Reynoso, L. Wence-Chávez, A. R. Arredondo-Valdez, S. Dumois-Petersen, Patricio Barros-Núñez, M. Gallegos-Arreola, S. Flores-Martínez, José Sánchez-Corona
{"title":"PPARD +294 T/C (rs2016520)多态性在墨西哥结直肠癌患者中的保护作用","authors":"M. A. Rosales-Reynoso, L. Wence-Chávez, A. R. Arredondo-Valdez, S. Dumois-Petersen, Patricio Barros-Núñez, M. Gallegos-Arreola, S. Flores-Martínez, José Sánchez-Corona","doi":"10.4238/gmr16019324","DOIUrl":null,"url":null,"abstract":"PPARD encodes for peroxisome proliferator-activated receptor delta, which plays a significant role in controlling lipid metabolism, atherosclerosis, inflammation, cancer growth, progression, and apoptosis. Accumulated evidence suggests that the polymorphism rs2016520 in PPARD is associated with lipid metabolism, obesity, metabolic syndrome, and type 2 diabetes mellitus. The aim of this study was to determine whether the single nucleotide polymorphism +294T/C (rs2016520) in PPARD is associated with colorectal cancer (CRC) in the Mexican population. Genomic DNA from 178 CRC patients and 97 healthy blood donors was analyzed. The polymorphism was identified by the polymerase chain reaction-restriction fragment length polymorphism method. Results demonstrated that patients with the T/C genotype for the +294T/C (rs2016520) polymorphism present a protective role against CRC [odds ratio (OR) = 0.39; 95% confidence interval (CI) = 0.22-0.69; P = 0.0008]. This association was also evident for the T/C genotype in the stratified analysis by tumor-node-metastasis stages I+II (OR = 0.26, P = 0.0332) and III+IV (OR = 0.44, P = 0.0067). However, in the stratified analysis by tumor location, we observed an increased risk of rectal cancer (OR = 7.57, P = 0.0403) vs colon cancer (OR = 4.87, P = 0.234) in patients carrying the C/C genotype and under the dominant and recessive models of inheritance. In conclusion, for the first time, the association between the +294T/C (rs2016520) polymorphism and colorectal cancer has been studied in Mexican patients. Our results reveal that variations in PPARD may play a significant role in genetic susceptibility to colorectal cancer.","PeriodicalId":189314,"journal":{"name":"Genetics and molecular research : GMR","volume":"33 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"2017-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"5","resultStr":"{\"title\":\"Protective role of +294 T/C (rs2016520) polymorphism of PPARD in Mexican patients with colorectal cancer.\",\"authors\":\"M. A. Rosales-Reynoso, L. Wence-Chávez, A. R. Arredondo-Valdez, S. Dumois-Petersen, Patricio Barros-Núñez, M. Gallegos-Arreola, S. Flores-Martínez, José Sánchez-Corona\",\"doi\":\"10.4238/gmr16019324\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"PPARD encodes for peroxisome proliferator-activated receptor delta, which plays a significant role in controlling lipid metabolism, atherosclerosis, inflammation, cancer growth, progression, and apoptosis. Accumulated evidence suggests that the polymorphism rs2016520 in PPARD is associated with lipid metabolism, obesity, metabolic syndrome, and type 2 diabetes mellitus. The aim of this study was to determine whether the single nucleotide polymorphism +294T/C (rs2016520) in PPARD is associated with colorectal cancer (CRC) in the Mexican population. Genomic DNA from 178 CRC patients and 97 healthy blood donors was analyzed. The polymorphism was identified by the polymerase chain reaction-restriction fragment length polymorphism method. Results demonstrated that patients with the T/C genotype for the +294T/C (rs2016520) polymorphism present a protective role against CRC [odds ratio (OR) = 0.39; 95% confidence interval (CI) = 0.22-0.69; P = 0.0008]. This association was also evident for the T/C genotype in the stratified analysis by tumor-node-metastasis stages I+II (OR = 0.26, P = 0.0332) and III+IV (OR = 0.44, P = 0.0067). However, in the stratified analysis by tumor location, we observed an increased risk of rectal cancer (OR = 7.57, P = 0.0403) vs colon cancer (OR = 4.87, P = 0.234) in patients carrying the C/C genotype and under the dominant and recessive models of inheritance. In conclusion, for the first time, the association between the +294T/C (rs2016520) polymorphism and colorectal cancer has been studied in Mexican patients. 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引用次数: 5
摘要
PPARD编码过氧化物酶体增殖物激活受体,在控制脂质代谢、动脉粥样硬化、炎症、癌症生长、进展和细胞凋亡中起重要作用。越来越多的证据表明PPARD中rs2016520多态性与脂质代谢、肥胖、代谢综合征和2型糖尿病有关。本研究的目的是确定PPARD中单核苷酸多态性+294T/C (rs2016520)是否与墨西哥人群的结直肠癌(CRC)相关。分析了178例结直肠癌患者和97名健康献血者的基因组DNA。采用聚合酶链反应-限制性片段长度多态性法鉴定其多态性。结果表明,T/C基因型+294T/C (rs2016520)多态性的患者对CRC具有保护作用[优势比(OR) = 0.39;95%置信区间(CI) = 0.22-0.69;P = 0.0008]。在肿瘤淋巴结转移分期I+II (OR = 0.26, P = 0.0332)和III+IV (OR = 0.44, P = 0.0067)的分层分析中,T/C基因型的相关性也很明显。然而,在肿瘤位置分层分析中,我们观察到携带C/C基因型的患者在显性和隐性遗传模式下患直肠癌的风险(OR = 7.57, P = 0.0403)高于结肠癌(OR = 4.87, P = 0.234)。总之,我们首次在墨西哥患者中研究了+294T/C (rs2016520)多态性与结直肠癌之间的关系。我们的研究结果表明PPARD的变异可能在结直肠癌的遗传易感性中起重要作用。
Protective role of +294 T/C (rs2016520) polymorphism of PPARD in Mexican patients with colorectal cancer.
PPARD encodes for peroxisome proliferator-activated receptor delta, which plays a significant role in controlling lipid metabolism, atherosclerosis, inflammation, cancer growth, progression, and apoptosis. Accumulated evidence suggests that the polymorphism rs2016520 in PPARD is associated with lipid metabolism, obesity, metabolic syndrome, and type 2 diabetes mellitus. The aim of this study was to determine whether the single nucleotide polymorphism +294T/C (rs2016520) in PPARD is associated with colorectal cancer (CRC) in the Mexican population. Genomic DNA from 178 CRC patients and 97 healthy blood donors was analyzed. The polymorphism was identified by the polymerase chain reaction-restriction fragment length polymorphism method. Results demonstrated that patients with the T/C genotype for the +294T/C (rs2016520) polymorphism present a protective role against CRC [odds ratio (OR) = 0.39; 95% confidence interval (CI) = 0.22-0.69; P = 0.0008]. This association was also evident for the T/C genotype in the stratified analysis by tumor-node-metastasis stages I+II (OR = 0.26, P = 0.0332) and III+IV (OR = 0.44, P = 0.0067). However, in the stratified analysis by tumor location, we observed an increased risk of rectal cancer (OR = 7.57, P = 0.0403) vs colon cancer (OR = 4.87, P = 0.234) in patients carrying the C/C genotype and under the dominant and recessive models of inheritance. In conclusion, for the first time, the association between the +294T/C (rs2016520) polymorphism and colorectal cancer has been studied in Mexican patients. Our results reveal that variations in PPARD may play a significant role in genetic susceptibility to colorectal cancer.