Association of Smoking and XPG, CYP1A1, OGG1, ERCC5, ERCC1, MMP2, and MMP9 Gene Polymorphisms with the early detection and occurrence of Laryngeal Squamous Carcinoma

Abstract

A total of 200 smoking-related laryngeal carcinoma patients with pathology confirmation from the Eye and ENT Hospital and 190 high-risk smokers were included in a survey. All of the participants had a smoking index greater than 400 (cigarettes/day*year.) We obtained data on clinical and baseline characteristics, and peripheral blood was obtained and subjected to DNA extraction to analyse the correlation between smoking and the occurrence of laryngeal carcinoma. We selected candidate genes and SNP fragments that were found to be closely associated with smoking-related tumours in preliminary studies. The selected candidate genes were XPG, CYP1A1, OGG1, ERCC5, ERCC1, MMP2, and MMP9. We then performed SNP sequencing using Sequenom SNP detection technology. Target genes and single nucleotide polymorphism (SNP) fragments were evaluated to analyse the correlation between genotype or allele and smoking-related laryngeal carcinoma and to identify susceptibility genes related to laryngeal carcinoma. The results included four main findings: (1) The smoking index differed significantly between laryngeal cancer patients and control subjects (P=0.0035). The risk of laryngeal cancer was increased among individuals with a smoking index greater than 600 cigarettes/day*year (P=0.03). (2) The smoking index was significantly correlated with the T, N and clinical stages (P<0.05). (3) The polymorphisms CYP1A1-rs1048943, rs4646421, and rs4646422 and MMP9-rs17577 were significantly associated with laryngeal squamous carcinoma (P<0.05). (4) After stratifying the subjects by smoking degree, the GT genotype of ERCC1-rs2298881 was associated with a significantly greater risk of laryngeal carcinoma among heavy smokers (P=0.04). The results suggest that smoking plays an important role in the occurrence and development of laryngeal squamous carcinoma; CYP1A1 and MMP9 might be susceptibility gene SNPs for smoking-related laryngeal carcinoma, and ERCC1 might play an important role in heavy smokers. The results of this study might help identify an early marker for the detection and prevention of laryngeal carcinoma.

Lower Expression of Gelsolin in Colon Cancer and Its Diagnostic Value in Colon Cancer Patients

“…Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases which are involved in multiple biological functions. Among MMPs, MMP2 and MMP9 were recognized as the key factors of cell migration in tumors 26-28. In this study, we found that the expression of MMP2 and MMP2 decreased on a dose dependent manner by recombinant GSN stimulation, which indicated that the secreted GSN could restrain the invasion and migration ability of colon cancer cells by decreasing the levels of MMP2 and MMP9.…”

Genotype of Null Polymorphisms in Genes GSTM1, GSTT1, CYP1A1, and CYP1A1*2A (rs4646903 T>C)/CYP1A1*2C (rs1048943 A>G) in Patients with Larynx Cancer in Southeast Spain

“…A study by Zhu Li et al investigated (SNP) polymorphisms for the genes XPG, CYP1A1, OGG1, ERCC5, ERCC1, MMP2 and MMP9 in a group of 200 patients with larynx cancer associated with heavy smoking in Shanghai (China), finding an association between SNP of genes CYP1A1 and MMP9 and larynx cancer. The authors proposed that these SNPs act as markers of an increased susceptibility to developing larynx cancer among smokers [ 64 ].…”

Lycopene Protects against Smoking-Induced Lung Cancer by Inducing Base Excision Repair

“…It is well established that tobacco exposure can reduce the expression of multiple DNA repair genes [50]. However, interestingly, our ANOVA results showed increased protein levels of OGG1 and NEIL2 as well as enhanced transcriptional level of NTH1 in the cells exposed to smoke compared with the non-smoking ones.…”

“…ATRA and β-carotene were dissolved in ethanol, while dimethyl sulfoxide (DMSO) was used as a carrier solvent for lycopene; cells were pretreated with these compounds at different doses (1 nM, 10 nM, 100 nM, 1 µM, and 10 µM) for 24 h. Then, lids of the plates were removed to expose lung cancer cells to one cigarette smoke from University of Kentucky research cigarettes (brand 1A1, 25 mg tar, 0.3 mg nicotine, [34]) using the chamber shown in Figure 1. The time-course experiment (10,20,30,40,50 and 60 min) was carried out to determine the optimal duration of exposure, leading to selecting a time point of 50 min, which was published previously [35,36].…”