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Thyrocyt e-specific deletion of insulin and IGF-1 receptors induces papillary thyroid carcinoma-like lesions through EGFR pathway activation

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Author(s)
Sangmi OckJihyun AhnSeok Hong LeeHyun Min KimHyun KangYoung-Kook KimHyun KookWoo Jin ParkShin KimShioko KimuraChan Kwon JungMinho ShongMartin HolzenbergerE. Dale AbelTae Jin LeeBo Youn ChoHo-Shik Kim`Jaetaek Kim
Keimyung Author(s)
Kim, Shin
Department
Dept. of Immunology (면역학)
Journal Title
International Journal of Cancer
Issued Date
2018
Volume
143
Issue
10
Keyword
insulin receptorIGF-1 receptorthyroidfolliculogenesishyperplasia
Abstract
Insulin and insulin-like growth factor (IGF)-1 signaling in the thyroid are thought to be permissive for the coordinated regulation by thyroid-stimulating hormone (TSH) of thyrocyte proliferation and hormone production. However, the integrated role of insulin receptor (IR) and IGF-1 receptor (IGF-1R) in thyroid development and function has not been explored. Here, we generated thyrocyte-specific IR and IGF-1R double knockout (DTIRKO) mice to precisely evaluate the coordinated functions of these receptors in the thyroid of neonates and adults. Neonatal DTIRKO mice displayed smaller thyroids, paralleling defective folliculogenesis associated with repression of the thyroid-specific transcription factor Foxe1. By contrast, at postnatal day 14, absence of IR and IGF-1R paradoxically induced thyrocyte proliferation, which was mediated by mTOR-dependent signaling pathways. Furthermore, we found elevated production of TSH during the development of follicular hyperplasia at 8 weeks of age. By 50 weeks, all DTIRKO mice developed papillary thyroid carcinoma (PTC)-like lesions that correlated with induction of the ErbB pathway. Taken together, these data define a critical role for IR and IGF-1R in neonatal thyroid folliculogenesis. They also reveal an important reciprocal relationship between IR/IGF-1R and TSH/ErbB signaling in the pathogenesis of thyroid follicular hyperplasia and, possibly, of papillary carcinoma.
Keimyung Author(s)(Kor)
김신
Publisher
School of Medicine (의과대학)
Citation
Sangmi Ock et al. (2018). Thyrocyt e-specific deletion of insulin and IGF-1 receptors induces papillary thyroid carcinoma-like lesions through EGFR pathway activation. International Journal of Cancer, 143(10), 2458–2469. doi: 10.1002/ijc.31779
Type
Article
ISSN
1097-0215
Source
https://onlinelibrary.wiley.com/doi/full/10.1002/ijc.31779
DOI
10.1002/ijc.31779
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/41745
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
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