Dataset Information

Association of the rs2071559 (T/C) polymorphism with lymphatic metastasis in patients with nasopharyngeal carcinoma.

ABSTRACT: Vascular endothelial growth factor (VEGF) and its receptor, VEGFR2, serve a critical role in angiogenesis and lymphangiogenesis, which are involved in the initiation and progression of malignancies. Specific single nucleotide polymorphisms of VEGF and VEGFR2 have been shown to modulate gene expression and influence malignancy aggressiveness. The aim of the present study was to determine whether the VEGFR2 rs2071559 (T/C) polymorphism is associated with the risk of developing nasopharyngeal carcinoma (NPC) and the aggressiveness of NPC in a southern Chinese population. A case-control study comprising 171 NPC patients and 184 healthy individuals was performed. Genotyping of the rs2071559 polymorphism was performed by quantitative polymerase chain reaction using TaqMan probes. Genotype and allele distribution of the rs2071559 polymorphism was not associated with the risk of NPC following adjustment for age, sex and ethnicity by multivariate logistic regression analyses. Regional lymph node metastasis was significantly correlated with the rs2071559 C allele and the related genotypes (OR 0.402, 95% CI 0.193-0.835, P=0.016; and OR 0.347, 95% CI 0.145-0.829, P=0.024, respectively). No correlations between genotype or allele distribution and the primary tumor size, distant metastasis, clinical stage, or histological type were observed. The rs2071559 polymorphism was shown to have an association with lymphatic metastasis in patients with NPC; however, the precise molecular mechanism should be elucidated in additional studies.

SUBMITTER: Hu K

PROVIDER: S-EPMC5755165 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature

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Association of the rs2071559 (T/C) polymorphism with lymphatic metastasis in patients with nasopharyngeal carcinoma.

Hu Kai K Xie Xiujing X Wang Rensheng R Wu Fang F Zhang Yong Y

Oncology letters 20171018 6

Vascular endothelial growth factor (VEGF) and its receptor, VEGFR2, serve a critical role in angiogenesis and lymphangiogenesis, which are involved in the initiation and progression of malignancies. Specific single nucleotide polymorphisms of VEGF and VEGFR2 have been shown to modulate gene expression and influence malignancy aggressiveness. The aim of the present study was to determine whether the VEGFR2 rs2071559 (T/C) polymorphism is associated with the risk ...[more]

PMID: 29344214

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Project description:BACKGROUND: Mitochondrial proteomic alterations of nasopharyngeal carcinoma metastasis remain unknown. Our purpose is to screen mitochondrial proteins for the elucidation of the molecular mechanisms of nasopharyngeal carcinoma metastasis and the discovery of metastasis-related biomarkers. METHODS: Mitochondria were isolated from nasopharyngeal carcinoma metastatic (5-8F) and nonmetastatic (6-10B) cell lines, respectively. After characterization of isolated mitochondria, mitochondrial differentially expressed proteins (DEPs) were quantified by two-dimensional difference in-gel electrophoresis (2D-DIGE), and identified by peptide mass fingerprint (PMF) and tandem mass spectrometry (MS/MS). A functional enrichment analysis and a protein-protein interaction sub-network analysis for DEPs were carried out with bioinformatics. Furthermore, siRNAs transient transfections were used to suppress expressions of some up-regulated DEPs in metastatic cells (5-8F), followed by Transwell Migration assay. RESULTS: Sixteen mitochondrial DEPs including PRDX3 and SOD2 were identified. Those 5-8F cells with suppression of PRDX3 showed an increased mobility potential. The functional enrichment analyses of DEPs discovered five significant biological processes including cellular response to reactive oxygen species, hydrogen peroxide metabolic process, regulation of mitochondrial membrane potential, cell redox homeostasis and oxidation reduction, and five significant molecular functions including oxidoreductase activity, caspase inhibitor activity, peroxiredoxin activity, porin activity and antioxidant activity. A protein-protein interaction sub-network of DEPs was generated with literature data. Ten mitochondrial DEPs including PRDX3, PRDX6, SOD2, ECH1, SERPINB5, COX5A, PDIA5, EIF5A, IDH3B, and PSMC4 were rationalized in the tumor-stroma co-evolution model that mitochondrial oxidative stress directly contributes to tumor metastasis. CONCLUSIONS: Sixteen mitochondrial DEPs were identified with mass spectrometry and ten of them were rationalized in the tumor-stroma co-evolution model. Those 5-8F cells with suppression of PRDX3 showed an increased mobility potential. These data suggest that those mitochondrial DEPs are potential biomarkers for NPC metastasis, and their dysregulation would play important roles in mitochondria oxidative stress-mediated NPC metastatic process.

Project description:p53 and glutathione S-transferase M1 (GSTM1) are the most popular suppressor genes. Several previous studies demonstrated positive associations of these gene polymorphisms with numerous cancer types, including hepatocellular cancer, while the association between p53/GSTM1 polymorphisms and the nasopharyngeal carcinoma (NPC) risk was inconsistent and underpowered. However, no studies investigating the combinational effect of these two genes on NPC risk were performed. To confirm the effects of p53 and GSTM1 polymorphisms on the risk of NPC, a meta-analysis of all the available previous studies associating p53 and GSTM1 with the risk of NPC was performed. A comprehensive search of PubMed, Web of Science and SD database until November 2014 was performed to identify the relevant studies. The data were extracted by two independent authors and pooled odds ratio (OR) with 95% confidence interval (CI) was calculated. Meta-regression and subgroup analyses were performed to identify the source of heterogeneity. Finally, five studies with 1,419 cases and 1,707 controls were included for the p53 polymorphism and three studies with 837 cases and 1,299 controls were included for the GSTM1 polymorphism. Regarding p53, a significantly increased NPC risk was observed in the overall population (C vs. G, OR, 1.245; 95% CI, 1.045-1.483; P=0.014; additive models: CC vs. GG, OR, 1.579; 95% CI, 1.100-2.265; P=0.013 and CG vs. GG, OR, 1.230; 95% CI, 1.039-1.456; P=0.016; dominant model, OR, 1.321; 95% CI, 1.127-1.549; P=0.001; recessive model, OR, 1.429; 95% CI, 1.017-2.009; P=0.040). Concerning GSTM1, a significantly increased NPC risk was observed in the overall population (null versus non-null, OR, 1.282; 95% CI, 1.075-1.530; P=0.006). In the subgroup analyses stratified by the source of controls, a significant association of p53 with NPC risk was also demonstrated, while no association with GSTM1 was observed. Therefore, the p53 G72C polymorphism may have a susceptible role in the carcinogenesis of NPC, while genetic deletion of GSTM1 may contribute to increased susceptibility to NPC. Further large and well-designed studies are required to confirm this association.

Dataset Information

Association of the rs2071559 (T/C) polymorphism with lymphatic metastasis in patients with nasopharyngeal carcinoma.

Publications

Association of the rs2071559 (T/C) polymorphism with lymphatic metastasis in patients with nasopharyngeal carcinoma.

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