Expression level of long non-coding RNA colon adenocarcinoma hypermethylated serve as a novel prognostic biomarker in patients with thyroid carcinoma
This study attempts to identify the prognostic value and potential mechanism of action of colorectal adenocarcinoma hypermethylated(CAHM) in thyroid carcinoma(THCA) by using the RNA sequencing dataset from The Cancer Genome Atlas(TCGA). The functional mechanism of CAHM was explored by using RNA sequencing dataset and multiple functional enrichment analysis approaches. Connectivity map online analysis tool was also used to predict CAHM targeted drugs. Survival analysis suggests that THCA patients with high CAHM expression have lower risk of death than these low CAHM expression(Log-rank P=0.022, adjusted P=0.011, HR=0.187, 95%CI=0.051-0.685). Function enrichment of CAHM co-expression genes suggests that CAHM may play a role in the following biological processes: DNA repair, cell adhesion, DNA replication, vascular endothelial growth factor receptor, Erb-B2 receptor tyrosine kinase 2, ErbB and thyroid hormone signaling pathways. Function enrichment of DEGs between low- and high-CAHM phenotype suggests that different CAHM expression levels may have the following differences in biological processes in THCA: cell adhesion, cell proliferation, extracellular signal regulated kinase 1(ERK1) and ERK2 cascade, G-protein coupled receptor, chemokine, and phosphatidylinositol-3-kinase-Akt signaling pathways. Connectivity map have identified five drugs (levobunolol, NU-1025, quipazine, anisomycin and sulfathiazole) for CAHM targeted therapy in THCA. Gene set enrichment analysis suggest that low CAHM phenotype were notably enriched in p53, nuclear factor kappa B, Janus kinase-signal transducer and activators of transcription, tumor necrosis factor, epidermal growth factor receptor and other signaling pathways. In the present study, we have identified CAHM may be serve as a novel prognostic biomarkers for predicting overall survival in patients with THCA.