ArticleJournal of Cancer2025
Hypoxia upregulate TPM4 expression to strengthen epithelial-mesenchymal transition that promotes lymph node metastasis of papillary thyroid cancer.
Article in Journal of Cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Impact of carbon-ion radiotherapy on tumor hypoxia detected byEuropean journal of nuclear medicine and molecular imaging · 2026Article
- Advances in immunotherapy for thyroid malignancies: from molecular targets to clinical outcomes.Frontiers in medicine · 2026Review
- Preoperative Circulating Tumor Cells (CTCs) Positivity is Associated with Lymph Node Metastasis in Patients with Unifocal Papillary Thyroid Microcarcinoma (PTMC).International journal of general medicine · 2026Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Papillary thyroid cancer (PTC) exhibits a high propensity for lymph node metastasis (LNM), significantly impacting postoperative recurrence and patient prognosis. The hypoxic microenvironment critically drives tumor progression by promoting PTC dedifferentiation. Through integrated bioinformatics analysis combining weighted gene co-expression network analysis and machine learning approaches on TCGA data, we identified TPM4 as a key hypoxia-responsive gene in PTC and validated its association with LNM using GEO datasets. Gene set enrichment analysis demonstrated that patients with high TPM4 expression in both TCGA and GEO databases showed significant enrichment in hypoxia and epithelial-mesenchymal transition (EMT) pathways. Single-cell pseudotime analysis revealed concurrent increases in hypoxia pathway enrichment, TPM4 expression, and EMT pathway activation during cell differentiation. Experimental validation using RT-qPCR and Western blot analyses confirmed that hypoxia-induced TPM4 upregulation activated EMT signaling. Functional assays demonstrated that TPM4 enhanced cellular invasion and migration capabilities. Our findings illuminate a novel mechanism whereby the hypoxic tumor microenvironment promotes lymph node metastasis in PTC through TPM4-mediated activation of EMT signaling, providing new insights into LNM of PTC.
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