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Investigating the mechanisms of papillary thyroid carcinoma using transcriptome analysis
Jie Qiu1, Wenwei Zhang2, Qingsheng Xia3
1Otolaryngology Head and Neck Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, P.R. China.
Molecular Medicine Reports
|August 30, 2017
Summary
This study identified key genes and transcriptomic changes in papillary thyroid cancer (PTC). Transforming growth factor β receptor 1 (TGFβR1) and NKX2-1-SFTA3 gene fusions may play roles in PTC development.
Area of Science:
- Oncology
- Genomics
- Molecular Biology
Background:
- Papillary thyroid cancer (PTC) is the most common type of thyroid cancer, accounting for 75-85% of cases.
- Understanding the transcriptomic landscape and genetic alterations in PTC is crucial for identifying potential therapeutic targets and understanding disease mechanisms.
Purpose of the Study:
- To investigate transcriptomic alterations and identify key genes involved in papillary thyroid cancer (PTC).
- To analyze single nucleotide polymorphisms (SNPs), differentially expressed genes (DEGs), and gene fusion events in PTC tissues.
Main Methods:
- RNA sequencing was employed to profile transcriptional changes in PTC and adjacent normal tissues.
- Bioinformatic analyses including SNP identification, DEG selection, enrichment analysis, and protein-protein interaction (PPI) network construction were performed.
- Gene fusion events were predicted using FusionMap software.
Main Results:
- A total of 70,172 SNPs and 2,686 DEGs were identified in tumor tissues.
- Fibronectin 1 (FN1) and transforming growth factor β receptor 1 (TGFβR1) showed high degrees in the PPI network.
- Seven PPI pairs with non-synonymous risk SNPs in interaction domains were found, notably involving FN1 and tenascin C (TNC).
- Eleven gene fusions were identified in tumor tissues, including NK2 homeobox 1-surfactant associated 3 (NKX2-1-SFTA3) in both tumor and normal tissues.
Conclusions:
- TGFβR1 and the NKX2-1-SFTA3 gene fusion are potentially implicated in the pathogenesis of PTC.
- Interactions between FN1 and TNC, particularly those involving non-synonymous risk SNPs, may contribute to PTC development.
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