ArticleFrontiers in endocrinology2022
Vitamin D Reduces Thyroid Cancer Cells Migration Independently From the Modulation of CCL2 and CXCL8 Chemokines Secretion.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.
- Vitamin D-Related Genes and Thyroid Cancer-A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Vitamin D decreases tumor cell growth and invasiveness in primary malignant bone tumors in vitro.Journal of bone oncology · 2026Article
- Vitamin D as a central modulator of thyroid diseases: mechanisms and clinical implications.Frontiers in immunology · 2026Review
- Vitamin D in Endocrine Disorders: A Broad Overview of Evidence in Musculoskeletal, Thyroid, Parathyroid, and Reproductive Disorders.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Tumor-associated macrophages as a potential therapeutic target in thyroid cancers.Cancer immunology, immunotherapy : CII · 2023Review
- Vitamin D deficiency linked to abnormal bone and lipid metabolism predicts high-risk multiple myeloma with poorer prognosis.Frontiers in endocrinology · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Vitamin D3 is largely involved in the regulation of calcium homeostasis. More recently, it was demonstrated that vitamin D exerts several beneficial effects against cancer progression through several mechanisms, including the reduction of cancer cells proliferation and migration. CXCL8 and CCL2 are two chemokines secreted by thyroid tumor cells. In the thyroid tumor microenvironment, these chemokines exert several pro-tumorigenic effects including the one to increase the metastatic potential. The aim of the present study was to investigate if vitamin D could modulate both thyroid cancer cell migration and their ability to secrete CCL2 and CXCL8. Methods: TPC-1 (RET/PTC rearranged) and 8505C (BRAFV600e mutated) thyroid cancer cell lines were treated with increasing concentrations of 1,25-OH-vitamin D3 (0-1,000 nM). Cell viability was assessed by WST-1 assay, cell migration was evaluated by transwell-migration chamber system, and CCL2 and CXCL8 levels were measured in the cell culture supernatants by ELISA. Results: Vitamin D did not affect cell viability but reduced, in a dose-dependent and significant manner, thyroid cancer cell migration (ANOVAs Conclusions: Vitamin D treatment of thyroid cancer cell lines reduces cell migration independently from the inhibition of the secretion of pro-tumorigenic chemokines. Future studies specifically designed at clarifying the pathways involved in the different inhibitory effects of vitamin D on CCL2 and CXCL8 in thyroid cancer cells appear worthwhile.
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