ArticleClinical and experimental medicine2025
Identification and functional characterization of hub genes CLTA, EDIL3, HAPLN1, and HIP1 as diagnostic biomarkers and therapeutic targets in thyroid cancer and Hashimoto's thyroiditis.
Article in Clinical and experimental medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Hashimoto's thyroiditis both promotes and protects against papillary thyroid cancer.Frontiers in endocrinology · 2026Review
- Precision Thyroid Oncology: A Review of Multi-Omics Biomarkers and Spatiotemporal Technologies.International journal of general medicine · 2026Review
- Epigenetic Mechanisms in Autoimmune Thyroid Diseases: Bridging Research and Clinical Applications.International journal of molecular sciences · 2025Review
- C3G deregulation uncovers a dual role in B-cell lymphoma: tumor suppression and enhanced metastasis via Rap1 and Rac2 signaling.Cell communication and signaling : CCS · 2025Article
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Authors and funding
6 authors.
Funding
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Abstract
In this study, we sought to identify key molecular players in both thyroid cancer (TC) and Hashimoto's thyroiditis (HT) by analyzing differentially expressed genes (DEGs) and their potential as biomarkers. We utilized datasets from the Gene Expression Omnibus (GEO) database and identified CLTA, EDIL3, HAPLN1, and HIP1 as hub genes common to both TC and HT. These genes were significantly upregulated in TC cell lines compared to normal controls, with high diagnostic accuracy as indicated by Receiver Operating Characteristic (ROC) curve analysis. Further validation using the TCGA TC dataset revealed their significant upregulation in tumor tissues, particularly in advanced TC stages. Promoter methylation analysis indicated hypomethylation of these genes in TC, suggesting a role of methylation in their regulation. We also observed mutations and copy number variations (CNVs) in these hub genes, with CLTA and HIP1 showing significant amplifications, which may contribute to their overexpression in tumor samples. In addition, we conducted a meta-analysis to assess the impact of these genes on survival outcomes in TC patients, with results indicating that higher expression of HAPLN1 and HIP1 was associated with poor survival. Our study also highlighted the involvement of CLTA and EDIL3 in activating the Rap1 signaling pathway, crucial for cancer cell migration, proliferation, and invasion. These findings emphasize the potential of CLTA, EDIL3, HAPLN1, and HIP1 as diagnostic biomarkers and therapeutic targets for TC and HT.
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