Abstract
Thyroid carcinoma is the most prevalent endocrine cancer globally and the primary cause of cancer-related mortality. Epigenetic modifications are progressively being linked to metastasis. This study aimed to examine whole-genome DNA methylation patterns and the gene expression profiles in thyroid cancer tissue samples using a MethylationEPIC BeadChip (850K), RNA sequencing, and a targeted bisulfite sequencing assay. The results of the Illumina Infinium human methylation kit (850K) analyses identified differentially methylated CpG locations (DMPs) and differentially methylated CpG regions (DMRs) encompassing nearly the entire genome with high resolution and depth. Gene ontology and KEGG pathway analyses revealed that the genes associated with DMRs belonged to various domain-specific ontologies, including cell adhesion, molecule binding, and proliferation. The RNA-Seq study found 1627 differentially expressed genes, 1174 of which that were up-regulated and 453 of which that were down-regulated. The targeted bisulfite sequencing assay revealed that CHST2, DPP4, DUSP6, ITGA2, SLC1A5, TIAM1, TNIK, and ABTB2 methylation levels were dramatically lowered in thyroid cancer patients when compared to the controls, but GALNTL6, HTR7, SPOCD1, and GRM5 methylation levels were significantly raised. Our study revealed that the whole-genome DNA methylation patterns and gene expression profiles in thyroid cancer shed new light on the tumorigenesis of thyroid cancer.
Highlights
Thyroid carcinoma is currently considered to be induced by the multi-step process of carcinogenesis, in which cancer cells are formed from thyroid follicular cells via numerous incidences of genomic injury
To identify epigenetic alterations occurring in thyroid carcinoma patients, the genomewide methylation patterns were explored using the Illumina Infinium Human Methylation
We identified 43,653 significantly differentially methylated CpG positions (DMP), accounting for 6.10% of all possible differentially methylated CpG locations (DMPs), and 236 significantly differentially methylated CpG regions (DMR) accounting for 18.96% of all possible DMRs
Summary
Thyroid carcinoma is currently considered to be induced by the multi-step process of carcinogenesis, in which cancer cells are formed from thyroid follicular cells (thyroid epithelial cells) via numerous incidences of genomic injury. These injuries primarily occur in oncogenes and anti-oncogenes that promote proliferation or the development of malignant phenotypes, such as the ability to penetrate surrounding tissue or metastasize to distant organs [1,2]. Thyroid carcinomas are classified into several types, including well-differentiated thyroid carcinoma (WDTC), undifferentiated thyroid carcinoma (UTC), poorly differentiated thyroid carcinoma (PDTC), anaplastic thyroid carcinoma (ATC), and medullary thyroid cancer (MTC). A considerable proportion of patients with well-differentiated thyroid carcinoma are treated with a total thyroidectomy, including the excision of the anterior or central compartment lymph nodes, radioactive iodine therapy for abscission of metastases and thyroid remnants, and suppression of TSH with l-thyroxin [5]
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