Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
Carcinogenesis. 2010 Dec;31(12):2082-90. doi: 10.1093/carcin/bgq198. Epub 2010 Oct 8.
Human DEC1 (deleted in esophageal cancer 1) gene is located on chromosome 9q, a region frequently deleted in various types of human cancers, including squamous cell carcinoma of the head and neck (SCCHN). However, only one epidemiological study has evaluated the association between DEC1 polymorphisms and cancer risk. In this hospital-based case-control study, four potentially functional single-nucleotide polymorphisms -1628 G>A (rs1591420), -606 T>C [rs4978620, in complete linkage disequilibrium with -249T>C (rs2012775) and -122 G>A(rs2012566)], c.179 C>T p.Ala60Val (rs2269700) and 3' untranslated region-rs3750505 as well as the TP53 tumor suppressor gene codon 72 (Arg72Pro, rs1042522) polymorphism were genotyped in 1111 non-Hispanic Whites SCCHN patients and 1130 age-and sex-matched cancer-free controls. After adjustment for age, sex and smoking and drinking status, the variant -606CC (i.e. -249CC) homozygotes had a significantly reduced SCCHN risk (adjusted odds ratio = 0.71, 95% confidence interval = 0.52-0.99) compared with the -606TT homozygotes. Stratification analyses showed that a reduced risk associated with the -606CC genotype was more pronounced in subgroups of non-smokers, non-drinkers, younger subjects (defined as ≤57 years), carriers of the TP53 Arg/Arg (rs1042522) genotype, patients with oropharyngeal cancer or late-stage SCCHN. Further in silico analysis revealed that the -249 T-to-C change led to a gain of a transcription factor-binding site. Additional functional analysis showed that the -249T-to-C change significantly enhanced transcriptional activity of the DEC1 promoter and the DNA-protein-binding activity. We conclude that the DEC1 promoter -249 T>C (rs2012775) polymorphism is functional, modulating susceptibility to SCCHN among non-Hispanic Whites.
人类 DEC1(食管癌缺失 1 基因)位于染色体 9q 上,该区域在多种人类癌症中经常缺失,包括头颈部鳞状细胞癌(SCCHN)。然而,只有一项流行病学研究评估了 DEC1 多态性与癌症风险之间的关联。在这项基于医院的病例对照研究中,我们对四个潜在的功能性单核苷酸多态性 -1628 G>A(rs1591420)、-606 T>C[rs4978620,与-249T>C(rs2012775)和-122 G>A(rs2012566)完全连锁]、c.179 C>T p.Ala60Val(rs2269700)和 3'非翻译区-rs3750505 以及 TP53 肿瘤抑制基因密码子 72(Arg72Pro,rs1042522)多态性进行了基因分型,共纳入了 1111 名非西班牙裔白人 SCCHN 患者和 1130 名年龄和性别匹配的癌症对照组。在调整年龄、性别、吸烟和饮酒状态后,与-606TT 纯合子相比,-606CC(即-249CC)纯合子的 SCCHN 风险显著降低(调整后的比值比=0.71,95%置信区间=0.52-0.99)。分层分析表明,在非吸烟者、不饮酒者、年轻受试者(定义为≤57 岁)、TP53 Arg/Arg(rs1042522)基因型携带者、口咽癌或晚期 SCCHN 患者亚组中,与-606CC 基因型相关的风险降低更为明显。进一步的计算机分析显示,-249 T 到 C 的变化导致了转录因子结合位点的获得。额外的功能分析表明,-249T 到 C 的变化显著增强了 DEC1 启动子的转录活性和 DNA-蛋白质结合活性。我们得出结论,DEC1 启动子-249T>C(rs2012775)多态性是功能性的,调节了非西班牙裔白人 SCCHN 的易感性。