ArticleEndocrine connections2024
TGFBR3 inhibits progression of papillary thyroid cancer by inhibiting the PI3K/AKT pathway and EMT.
Article in Endocrine connections, 2024. 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.
- Platelet-rich plasma-derived exosomes establishing a muscular proregenerative microenvironment through enhancing the viability of fibro-adipogenic progenitors.Experimental & molecular medicine · 2025Article
- Personalized prediction of lymph node metastasis in papillary thyroid microcarcinoma: a nomogram and web calculator.Scientific reports · 2025Article
- The roles, signalling pathways and therapeutic implications of Apoc1 in cancer.Discover oncology · 2025Review
- CXCR7-TAGLN2 protein complex regulates invasion and metastasis in papillary thyroid carcinoma: a potential therapeutic target.Frontiers in immunology · 2025Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Transforming growth factor beta receptor III (TGFBR3) has been shown to play a tumor-suppressive role in a variety of cancers. However, its role in papillary thyroid cancer (PTC) remains unknown. Method: TGFBR3 expression levels in PTC were analyzed utilizing The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Edu, wound healing, and Transwell assays were used to evaluate cell proliferation, migration, and invasion. Transcriptome sequencing, quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR), and Western blotting were used to detect the underlying mechanism of TGFBR3 in PTC progression. Result: This study demonstrated that TGFBR3 expression was significantly down-regulated in PTC compared to normal thyroid tissues. Low expression of TGFBR3 was associated with poor prognosis of patients with PTC. Furthermore, TGFBR3 expression positively correlated with thyroid differentiation score. In investigating the biological impact of TGFBR3 overexpression in PTC cell lines, we found that the proliferation, migration, and invasion of PTC cells were significantly inhibited in response to TGFBR3 overexpression. Moreover, we also demonstrated that overexpression of TGFBR3 inhibited the PI3K/AKT pathway and epithelial-mesenchymal transformation processes. Lastly, TGFBR3 expression was found to be involved in tumor immune infiltration, highlighting its potential influence on immune dynamics within the tumor microenvironment in PTC. Conclusion: TGFBR3 plays a tumor-suppressive role in PTC progression by inhibiting the PI3K/AKT pathway and epithelial mesenchymal transformation.
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