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Therapeutic Potential of Sodium Selenite Application for Promoting Radioactive Iodine Avidity in Papillary Thyroid
Ji Min Oh1,2, Ramya Lakshmi Rajendran1,2,3, Prakash Gangadaran1,2
1Department of Nuclear Medicine, School of Medicine, Kyungpook National University, Daegu, 41944, Republic of Korea, knu.ac.kr.
Objective:
Radioactive iodine therapy is a mainstay for recurrent and metastatic differentiated thyroid cancer. However, a substantial portion of differentiated thyroid cancer patients exhibits dedifferentiation status with a lack of sodium iodide symporter functionality and expression, as well as downregulated thyroid-specific proteins and transcription factors. Eventually, this status is connected to the failure of radioactive iodine therapy with an overall poor prognosis. Selenium, an essential trace element, has antitumor, antioxidant, immunomodulatory, and antiviral activities and is required for thyroid hormone synthesis and metabolism, and it was reported that sodium selenite induces radioactive iodine uptake in thyroid tissue in rats. However, the relationship between sodium selenite and differentiation markers in differentiated thyroid cancer remains unclear.
Methods:
We investigated whether sodium selenite enhances radioactive iodine avidity and reinforces 131I therapeutic effects in papillary thyroid cancer cells. We also analyzed changes in selected signaling pathways and factors induced by sodium selenite treatment.
Results:
Sodium iodide symporter, thyroid-specific proteins, and transcription factors were upregulated by sodium selenite, increasing radioactive iodine avidity and radioactive iodine-mediated cytotoxicity in papillary thyroid cancer cells. Sodium selenite downregulated the MAPK, PI3K-AKT, and GSK-3β/β-catenin signaling pathways.
Conclusion:
Sodium selenite may serve as a promising adjunct to enhance radioactive iodine avidity in papillary thyroid cancer cells.
Insights
Sodium selenite may improve radioactive iodine therapy for differentiated thyroid cancer. It enhances radioactive iodine uptake and cancer cell killing by upregulating key markers and downregulating specific signaling pathways.
Area of Science:
- Oncology
- Endocrinology
- Molecular Biology
Background:
- Radioactive iodine therapy is crucial for differentiated thyroid cancer but often fails in dedifferentiated tumors.
- Dedifferentiation leads to reduced sodium iodide symporter expression and poor prognosis.
- Selenium's role in thyroid cancer and its potential to enhance radioactive iodine uptake require further investigation.
Purpose of the Study:
- To determine if sodium selenite enhances radioactive iodine avidity in papillary thyroid cancer cells.
- To assess the impact of sodium selenite on radioactive iodine therapeutic efficacy.
- To analyze signaling pathway alterations induced by sodium selenite.
Main Methods:
- Papillary thyroid cancer cells were treated with sodium selenite.
- Radioactive iodine avidity was measured.
- Expression of sodium iodide symporter, thyroid-specific proteins, and transcription factors was analyzed.
- Signaling pathways (MAPK, PI3K-AKT, GSK-3β/β-catenin) were assessed.
Main Results:
- Sodium selenite upregulated the sodium iodide symporter, thyroid-specific proteins, and transcription factors.
- This resulted in increased radioactive iodine avidity and cytotoxicity.
- Sodium selenite downregulated MAPK, PI3K-AKT, and GSK-3β/β-catenin signaling pathways.
Conclusions:
- Sodium selenite shows potential as an adjuvant therapy to improve radioactive iodine avidity in papillary thyroid cancer.
- It enhances the effectiveness of radioactive iodine treatment by modulating key cellular mechanisms.
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