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Wild-Type P53 Induces Sodium/Iodide Symporter Expression Allowing Radioiodide Therapy in Anaplastic Thyroid Cancer
Lin Liu1,2, Dan Li1, Zhengqi Chen3
1Department of Nuclear Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China.
Aims:
Anaplastic thyroid cancer(ATC) is one of the most aggressive solid tumors. Mutations in the p53 gene are common in anaplastic thyroid cancer, but the effects of p53 mutations are yet to be elucidated. Here, we investigated the role of p53 in ATC.
Methods:
p53 mutation was detect by immunohistochemistry in ATC tissues. Expression of NIS were measured using immunohistochemistry, qRT-PCR, western blot, immunofluorescence in ATC tissues and cell line 8505c. Luciferase reporter assay was performed to examine the effect of wild-type p53 on NIS. Radioiodide uptake assay and flow cytometry analysis were used to detect the role of wild-type p53 on radioiodide uptake.and cell apoptosis in ATC cell line.
Results:
We showed that the p53 mutation can be detected in ATC tissues. Furthermore, we demonstrated that wild-type p53 transactivated the NIS promoter. In 8505c cells transfected with wild-type p53, treatment with radioiodine resulted in increased radioiodine uptake and increased apoptotic cell death compared with 8505c cells harboring the p53 mutation.
Conclusion:
In summary, transfection with wild-type p53 can increase the therapeutic effect of radioiodine by regulating the expression of the NIS.
Insights
Restoring wild-type p53 in anaplastic thyroid cancer (ATC) enhances radioiodine therapy by increasing sodium-iodide symporter (NIS) expression, leading to greater radioiodide uptake and cancer cell death.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Anaplastic thyroid cancer (ATC) is an aggressive malignancy with frequent p53 gene mutations.
- The precise role of p53 mutations in ATC pathogenesis and treatment response remains unclear.
Purpose of the Study:
- To investigate the functional role of p53 in anaplastic thyroid cancer.
- To determine the impact of wild-type p53 on sodium-iodide symporter (NIS) expression and radioiodide uptake in ATC.
Main Methods:
- Immunohistochemistry, qRT-PCR, Western blot, and immunofluorescence were used to detect p53 and NIS expression in ATC tissues and cell lines.
- Luciferase reporter assays assessed wild-type p53's effect on the NIS promoter.
- Radioiodide uptake assays and flow cytometry evaluated the impact of p53 status on radioiodine efficacy and apoptosis.
Main Results:
- p53 mutations were confirmed in ATC tissues.
- Wild-type p53 was shown to transactivate the NIS promoter, upregulating NIS expression.
- Restoration of wild-type p53 in ATC cells increased radioiodine uptake and induced significant apoptotic cell death.
Conclusions:
- Wild-type p53 plays a crucial role in regulating NIS expression in anaplastic thyroid cancer.
- Restoring wild-type p53 function can enhance the therapeutic efficacy of radioiodine treatment in ATC by modulating NIS levels.
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