Abstract
BackgroundTriggering receptor expressed on myeloid cells-1 (TREM-1) has been reported as a biomarker in many cancers. However, the biological function of TREM-1 in papillary thyroid carcinoma (PTC) remains unknown.MethodsWe obtained TREM-1 expression data from The Cancer Genome Atlas (TCGA) database. Enrichment analysis of coexpressed genes and TREM-1 methylation analysis were performed via LinkedOmics. The correlations between TREM-1 and immune infiltrates were investigated via ESTIMATE, TIMER and TISIDB. We analyzed the association of TREM-1 expression with pan-cancer overall survival via Gene Expression Profiling Interactive Analysis (GEPIA).Results TREM-1 has lower methylation levels and higher expression levels in PTC tissues compared to normal tissues. TREM-1 expression is significantly associated with poor prognosis, advanced T classification, advanced N classification, and an increased incidence of BRCA2 and BRAF mutations. Genes coexpressed with TREM-1 primarily participate in immune-related pathways. TREM-1 expression is positively correlated with immune infiltration, tumor progression and poor overall survival across cancers.ConclusionsTREM-1 is a good prognostic and diagnostic biomarker in PTC. TREM-1 may promote thyroid cancer progression through immune-related pathways. Methylation may act as an upstream regulator of TREM-1 expression and biological function. Additionally, TREM-1 has broad prognostic value in a pan-cancer cohort.
Highlights
Thyroid carcinoma [1] is the most prevalent endocrine malignancy, and its global incidence has rapidly increased in recent decades [2]
We initially evaluated Triggering receptor expressed on myeloid cells-1 (TREM-1) mRNA levels in Papillary thyroid carcinoma (PTC) tissues from The Cancer Genome Atlas (TCGA)
Receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic value of TREM-1 using data from Gene Expression Omnibus (GEO) cohorts (Figures 1J–O)
Summary
Thyroid carcinoma [1] is the most prevalent endocrine malignancy, and its global incidence has rapidly increased in recent decades [2]. TREM-1 is highly expressed by neutrophils and epithelial cells in skin and lymph nodes infected with bacteria or fungi [8]. A previous study has indicated that lung cancer cells upregulate TREM-1 expression and that tumor-associated macrophages have increased levels of TREM-1 [10]. Functional experiments involving hepatocellular carcinoma (HCC) have suggested that TREM-1 promotes proliferation, increases invasiveness and inhibits apoptosis of HCC cells [11, 12]. TREM-1 is induced in macrophages by the androgen receptor signaling pathway in prostate cancer, and increases the motility and invasive capacity of prostate cancer cells [16]. Triggering receptor expressed on myeloid cells-1 (TREM-1) has been reported as a biomarker in many cancers. The biological function of TREM-1 in papillary thyroid carcinoma (PTC) remains unknown
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