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The BRAF p.V600E mutation significantly drives thyroid cancer progression by activating the RAS/BRAF/MEK/ERK pathway. This activation results in cancer cell dedifferentiation, making many patients resistant to standard radioiodine therapy. However, researchers are exploring miR-335-5p thyroid cancer interactions as a method to resensitize these tumors. By using SWitchMiner software, scientists identified a small pool of switch genes associated with drastic phenotype changes. Specifically, miR-335-5p emerged as a critical regulator using transcriptomic data from papillary thyroid carcinoma.
Restoring this microRNA in BRAF-mutant cell lines increased the expression of thyroid-specific genes and proteins. This restoration enhanced the localization of the sodium-iodide symporter (NIS), which directly improved iodine uptake in organoids. Consequently, this process helps resensitize tumors to radioiodine therapy, which often remains the gold standard for management. Additionally, the study explored the connection between thyroid-specific genes and the epithelial-mesenchymal transition (EMT) pathway.
Because EMT pathways modulate resistance to kinase inhibitors (KI), inhibiting these genes is vital for clinical success. Notably, miR-335-5p inhibited nearly all analyzed EMT genes in less-differentiated thyroid cell lines. In fact, this dual action makes it a promising therapeutic target for advanced disease. Targeting this microRNA may provide a combined benefit by restoring radioiodine avidity and reducing treatment resistance. Therefore, physicians should consider these molecular findings when managing metastatic cases that no longer respond to conventional iodine therapy.
miR-335-5p acts as a regulatory switch that increases the expression of thyroid-specific genes. This process restores the localization of the sodium-iodide symporter (NIS), allowing cancer cells to once again absorb iodine.
The microRNA inhibits the Epithelial-Mesenchymal Transition (EMT) pathway. Since EMT is a major driver of resistance to kinase inhibitors, miR-335-5p can help enhance the efficacy of these targeted therapies.
This mutation triggers pathways that cause thyroid cells to lose their differentiated features. As a result, the cells lose the ability to take up iodine, leading to radioiodine-refractory metastatic disease.
Disclaimer: This content is for informational and educational purposes only. It does not constitute medical advice or a professional opinion. Readers should consult with a qualified healthcare professional for specific medical concerns. Refer to the latest local and national guidelines for clinical practice.
References
Pecce V et al. The role of miR-335-5p in the redifferentiation of BRAF p.V600E thyroid cancers. Mol Oncol. 2026 Jun 22. doi: 10.1002/1878-0261.70181. PMID: 42325083.
Zhang X, et al. MicroRNA-335-5p as a suppressor in various cancers: A comprehensive review. Cancer Cell Int. 2021;21:550.
Nanni S, et al. The BRAF inhibitor Dabrafenib in the redifferentiation of radioiodine-refractory thyroid cancer. Endocrine. 2022;75(2):481-490.
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Recent research identifies miR-335-5p as a key regulator for redifferentiating BRAF-mutant thyroid cancers. Restoring this microRNA enhances iodine uptake and inhibits EMT pathways, potentially resensitizing tumors to radioiodine and improving kinase inhibitor outcomes for refractory patients.
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