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Peer-reviewedCC BYFrontiers in immunology

Radioiodine-induced cGAS-STING signaling and antitumor immunity in thyroid cancer

  • Feng Gao1
  • Daoming Zhang1
  • Yan Luo2
  • Chunhua Li3
  1. 1Department of General Surgery, Affiliated Hospital of Changchun University of Chinese Medicine , ,
  2. 2Patient Services Center, Affiliated Hospital of Changchun University of Chinese Medicine , ,
  3. 3Department of Endocrinology and Metabolism, Affiliated Hospital of Changchun University of Chinese Medicine , ,
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Abstract

Radioiodine (RAI) is a cornerstone of treatment for differentiated thyroid cancer (DTC), yet the immunological consequences of RAI-induced DNA damage remain poorly understood. Here, we examine cGAS–STING signaling as a potential mechanistic link between RAI-induced genotoxic stress and antitumor immunity. RAI delivers prolonged, thyroid-selective radiation to iodine-avid tumors, providing a plausible source of extranuclear DNA capable of engaging innate DNA sensing. We propose that transient RAI-associated cGAS–STING activation in DTC may favor IRF3–type I interferon-dependent immune priming, whereas persistent genomic stress in RAI-refractory anaplastic and poorly differentiated thyroid cancers (ATC/PDTC) may shift pathway output toward NF-κB-dominated, myeloid-suppressive programs. This acute-versus-chronic framework suggests that cGAS–STING dynamics could help define a therapeutic window for sequencing RAI with immune checkpoint blockade, while controlled STING activation may provide an alternative strategy for iodine-refractory disease. Direct evidence for RAI-induced cGAS–STING activation in thyroid tumors remains lacking, highlighting the need to define pathway kinetics across thyroid cancer subtypes and determine whether thyroid-specific endocrine signaling, including TSH–TSHR signaling, further modulates innate DNA sensing.

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Cite

BibTeXRIS
BibTeX
@article{gao2026radioiodineinduced,
  title = {{Radioiodine-induced cGAS-STING signaling and antitumor immunity in thyroid cancer}},
  author = {Feng Gao and Daoming Zhang and Yan Luo and Chunhua Li},
  journal = {Frontiers in immunology},
  year = {2026},
  month = sep,
  doi = {10.3389/fimmu.2026.1985864},
  url = {https://europepmc.org/article/PMC/PMC13662556},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Radioiodine-induced cGAS-STING signaling and antitumor immunity in thyroid cancer
AU  - Feng Gao
AU  - Daoming Zhang
AU  - Yan Luo
AU  - Chunhua Li
PY  - 2026
DA  - 2026/09/30
JO  - Frontiers in immunology
DO  - 10.3389/fimmu.2026.1985864
UR  - https://europepmc.org/article/PMC/PMC13662556
AB  - Radioiodine (RAI) is a cornerstone of treatment for differentiated thyroid cancer (DTC), yet the immunological consequences of RAI-induced DNA damage remain poorly understood. Here, we examine cGAS–STING signaling as a potential mechanistic link between RAI-induced genotoxic stress and antitumor immunity. RAI delivers prolonged, thyroid-selective radiation to iodine-avid tumors, providing a plausible source of extranuclear DNA capable of engaging innate DNA sensing. We propose that transient RAI-associated cGAS–STING activation in DTC may favor IRF3–type I interferon-dependent immune priming, whereas persistent genomic stress in RAI-refractory anaplastic and poorly differentiated thyroid cancers (ATC/PDTC) may shift pathway output toward NF-κB-dominated, myeloid-suppressive programs. This acute-versus-chronic framework suggests that cGAS–STING dynamics could help define a therapeutic window for sequencing RAI with immune checkpoint blockade, while controlled STING activation may provide an alternative strategy for iodine-refractory disease. Direct evidence for RAI-induced cGAS–STING activation in thyroid tumors remains lacking, highlighting the need to define pathway kinetics across thyroid cancer subtypes and determine whether thyroid-specific endocrine signaling, including TSH–TSHR signaling, further modulates innate DNA sensing.
SN  - 1664-3224
ER  -