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Novel non-genomic signaling of thyroid hormone receptors in thyroid carcinogenesis
Molecular and Cellular Endocrinology, 06/25/09

Guigon CJ et al. – Review article highlights the recent advances in understanding of the critical role of novel non-genomic actions of mutations of thyroid hormone receptor (TR) in thyroid carcinogenesis.

Studies so far have shown that the deleterious effects of TRβ mutants in causing resistance to thyroid hormone (RTH) are mediated via dominant negative actions at the transcriptional level
However, novel modes of TRβ mutant actions have been identified from mice study that are beyond nucleus-initiated transcription:
- Direct protein–protein interaction with the PI3K leads to cell proliferation, apoptosis, migration, and metastasis
- Direct interation with PTTG or β-catenin affects their degradation by the proteasomal pathways, thus leading to PTTG and β-catenin aberrant accumulation
- This contributes to genetic instability and constitutively active β-catenin oncogenic signaling to affect cell proliferation and migration
Therefore, the development and progression of thyroid tumors in mice not only involve impaired transcriptional activity but also derailed post-transcriptional mechanisms

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