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TNFRSF12A is associated with immune cell infiltration in thyroid carcinoma
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Abstract
Objective: Comprehensively investigated the immune infiltration of thyroid cancer, to explore key immune-related genes and potential molecular mechanisms for thyroid carcinoma through bioinformatics analysis.
Methods: The thyroid carcinoma (THCA) expression profiles came from the Cancer Genome Atlas (TCGA) databases. The differences in the infiltration levels of immune cells between THCA were analyzed by the CIBERSORT. We analyzed the differentially expressed genes (DEGs) in thyroid, downloaded the immunologically relevant list of genes from IMMPORT, and then selected the differentially expressed immune genes. Gene ontology (GO) terms and pathways associated with these DEGs were identified, and protein–protein interactions (PPIs) were analyzed. The expression of TNFRSF12Ain THCA was analyzed in the cBioPortal database. Additionally, we used the Tumor Immune Estimation Resource (TIMER) database evaluated correlation between TNFRSF12A expression and immune cell infiltration.Finally, Kaplan-Meier survival analysis was presented to predict the survival times between high and low TNFRSF12A expression groups for THCA.
Results: Differentially expressed immune genes associated with prognosis included BMP2, SEMA6B, INHBB and TNFRSF12A. There were distinct differences in the infiltration levels of immune cells between THCA and normal tissues. TNFRSF12A was identified to be highly expressed in THCA compared to normal tissues. TNFRSF12A mutation occurred in 5% of THCA samples, and low mRNA expression was the most common type of mutation. TNFRSF12A expression was significantly correlated to the infiltration levels of B cells, CD8+ T cells, CD4+ T cells, neutrophils and dendritic cells. Gene Set Enrichment Analysis (GSEA) results indicated that TNFRSF12A could be involved in key biological processes and pathways of cytokine-cytokine receptor interaction. Patients with low TNFRSF12A expression usually experienced shorten overall survival time than those with its high expression.
Conclusion: Our findings revealed that TNFRSF12A was significantly related to immune cell infiltration, which may provide potential value for immunotherapy.
Title: TNFRSF12A is associated with immune cell infiltration in thyroid carcinoma
Description:
Abstract
Objective: Comprehensively investigated the immune infiltration of thyroid cancer, to explore key immune-related genes and potential molecular mechanisms for thyroid carcinoma through bioinformatics analysis.
Methods: The thyroid carcinoma (THCA) expression profiles came from the Cancer Genome Atlas (TCGA) databases.
The differences in the infiltration levels of immune cells between THCA were analyzed by the CIBERSORT.
We analyzed the differentially expressed genes (DEGs) in thyroid, downloaded the immunologically relevant list of genes from IMMPORT, and then selected the differentially expressed immune genes.
Gene ontology (GO) terms and pathways associated with these DEGs were identified, and protein–protein interactions (PPIs) were analyzed.
The expression of TNFRSF12Ain THCA was analyzed in the cBioPortal database.
Additionally, we used the Tumor Immune Estimation Resource (TIMER) database evaluated correlation between TNFRSF12A expression and immune cell infiltration.
Finally, Kaplan-Meier survival analysis was presented to predict the survival times between high and low TNFRSF12A expression groups for THCA.
Results: Differentially expressed immune genes associated with prognosis included BMP2, SEMA6B, INHBB and TNFRSF12A.
There were distinct differences in the infiltration levels of immune cells between THCA and normal tissues.
TNFRSF12A was identified to be highly expressed in THCA compared to normal tissues.
TNFRSF12A mutation occurred in 5% of THCA samples, and low mRNA expression was the most common type of mutation.
TNFRSF12A expression was significantly correlated to the infiltration levels of B cells, CD8+ T cells, CD4+ T cells, neutrophils and dendritic cells.
Gene Set Enrichment Analysis (GSEA) results indicated that TNFRSF12A could be involved in key biological processes and pathways of cytokine-cytokine receptor interaction.
Patients with low TNFRSF12A expression usually experienced shorten overall survival time than those with its high expression.
Conclusion: Our findings revealed that TNFRSF12A was significantly related to immune cell infiltration, which may provide potential value for immunotherapy.
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Disclosure: C.M. Mirano: None. R.C. Mirasol: None.
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