Abstract
Thyroid carcinoma (TC) is the most common endocrine malignancy, and papillary TC (PTC) is the most frequent subtype of TC, accounting for 85–90% of all the cases. Aberrant histone acetylation contributes to carcinogenesis by inducing the dysregulation of certain cancer-related genes. However, the histone acetylation landscape in PTC remains elusive. Here, we interrogated the epigenomes of PTC and benign thyroid nodule (BTN) tissues by applying H3K27ac chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) along with RNA-sequencing. By comparing the epigenomic features between PTC and BTN, we detected changes in H3K27ac levels at active regulatory regions, identified PTC-specific super-enhancer-associated genes involving immune-response and cancer-related pathways, and uncovered several genes that associated with disease-free survival of PTC. In summary, our data provided a genome-wide landscape of histone modification in PTC and demonstrated the role of enhancers in transcriptional regulations associated with prognosis of PTC.
Highlights
Thyroid carcinoma (TC) is the most common endocrine malignancy with an increasing incidence during the past decades (Kilfoy et al, 2009)
Principal component analysis (PCA) indicated that papillary TC (PTC) and benign thyroid nodule (BTN) samples grouped into two clusters according to their genome-wide H3K27ac profiles, suggesting that the differences were etiology specific (Figure 1A)
When comparing H3K27ac peaks between PTC and BTN, 395 peaks were unique to PTC samples, while 437 peaks were unique to BTN
Summary
Thyroid carcinoma (TC) is the most common endocrine malignancy with an increasing incidence during the past decades (Kilfoy et al, 2009). It is well accepted that both genetic alterations and epigenetic changes contribute to PTC development and progression. Some somatic driver mutations, such as the BRAF V600E and TERT promoter mutations (Liu et al, 2017), and epigenetic alterations, such as specific non-coding RNAs and DNA methylation modifications (Yu et al, 2012; Yim et al, 2019), have been well established as diagnostic and prognostic markers of PTC. Histones are subject to a variety of post-transcriptional modifications including methylation, acetylation, phosphorylation, and ubiquitination (Bártová et al, 2008; Matsuda et al, 2015), which influence interactions between DNA and histones, resulting in global regulation of gene expression. Histone acetylation is related to active transcription, while deacetylation
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