RESUMO
Aim: To assess the expression and effect of ELK3 in gastric cancer, along with its associations with the VEGF-C/VEGFR-3 axis, IC50 of the VEGFR-3 inhibitor axitinib and immune infiltration of M2-polarized macrophages in gastric cancer, and to analyze the possible epigenetic regulation mechanism. Materials & methods: Expression profiles and methylation data from 1645 samples were obtained and examined from multi-institutional public datasets. The associations were assessed by multiple analysis methods. Results: Elevated ELK3 is associated with the VEGF-C/VEGFR-3 axis and tumorigenesis, reduces the effect of axitinib in vitro, enhances immune infiltration of M2 macrophages and affects clinical outcomes. Hypomethylation contributes to the upregulation of ELK3 in gastric cancer. Conclusions:ELK3 is a potential therapeutic target which reduces the effect of axitinib and enhances infiltration of M2-polarized macrophages.
Assuntos
Macrófagos/metabolismo , Proteínas Proto-Oncogênicas c-ets/genética , Neoplasias Gástricas/genética , Fator C de Crescimento do Endotélio Vascular/genética , Receptor 3 de Fatores de Crescimento do Endotélio Vascular/genética , Idoso , Feminino , Humanos , Macrófagos/patologia , Masculino , Proteínas Proto-Oncogênicas c-ets/metabolismo , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Fator C de Crescimento do Endotélio Vascular/metabolismo , Receptor 3 de Fatores de Crescimento do Endotélio Vascular/metabolismoRESUMO
AIM: To assess SLC6A6 expression in gastric cancer, its correlation with patients' clinicopathological features and survival, and the possible epigenetic regulation mechanism. METHODS: Expression profiles and methylation data were obtained from the Gene Expression Omnibus database and the Cancer Genome Atlas. The SLC6A6's protein level were obtained from the Human Protein Atlas. Correlations between SLC6A6 expression and clinicopathological features were assessed using the χ2 test, and survival by the Kaplan-Meier analysis. By analyzing methylation data, the mechanisms of SLC6A6 dysregulation were investigated. RESULTS: SLC6A6 expression was higher in gastric cancer, and indicated poor prognosis. Low-methylation levels were significantly related to high SLC6A6 expression. CONCLUSION: SLC6A6 may be a potential prognostic marker and therapeutic target. Hypomethylation contributes to SLC6A6 upregulation in gastric cancer.
Assuntos
Biomarcadores Tumorais/metabolismo , Metilação de DNA , Regulação Neoplásica da Expressão Gênica , Glicoproteínas de Membrana/metabolismo , Proteínas de Membrana Transportadoras/metabolismo , Neoplasias Gástricas/mortalidade , Idoso , Biomarcadores Tumorais/genética , Carcinogênese , Estudos de Casos e Controles , Epigênese Genética , Feminino , Seguimentos , Humanos , Masculino , Glicoproteínas de Membrana/genética , Proteínas de Membrana Transportadoras/genética , Prognóstico , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia , Taxa de SobrevidaRESUMO
AIM: To investigate the expression of TRIP13 in multiple tumors and to evaluate the relationship between TRIP13 and survival of cancer patients. MATERIALS & METHODS: Sample expression profiles were downloaded from the gene expression omnibus database. Correlation between TRIP13 expression and clinicopathological features was analyzed by χ2 test. Patient survival was evaluated by Kaplan-Meier analysis. RESULTS: TRIP13 expression was upregulated in 12 cancer types; it significantly correlated with multiple clinicopathological features of breast, liver and lung cancer. High TRIP13 expression indicated poor prognosis of patients with breast, liver, gastric and lung cancer. CONCLUSION: TRIP13 is highly expressed in multiple tumors and may be used as a potential prognostic marker and therapeutic target.