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Central Laboratory, and
¹ Department of Endocrinology of Shandong Provincial Hospital, Shandong University, Jinan 250021, China
² Department of Neurology, Case Western Reserve University, Cleveland, Ohio 44106, USA

(Requests for offprints should be addressed to J Zhao; Email: jjzhao{at}medmail.com.cn)

(M Ren and Q B Guan contributed equally to this work)

It is known that decreased apoptosis of thyrocytes may be involved in the formation of goiters in patients with Graves’ disease, and growth factors are involved in regulating the size of the thyroid gland. The purpose of our study was to investigate mRNA and protein levels of an antiapoptotic protein, namely, Fas-associated death domain-like interleukin-1-converting enzyme (FLICE)-inhibitory protein (FLIP). The results showed that in FRTL thyroid cells, treatment with IGF-I upregulated mRNA and protein levels of FLIP in a dose-dependant manner. While a specific nuclear factor-B (NF-B) inhibitor, BAY11-7082, blocked this effect. Further study demonstrated that IGF-I induced the DNA-binding activity of NF-B in association with decreased expression of the NF-B inhibitory protein IB . These findings implied that IGF-I increased FLIP expression by enhancing the activation of NF-B in FRTL thyroid cells. Using a specific phosphatidylinositol 3-kinase (PI3K) inhibitor, LY294002, we also found that PI3K was involved in the pathway by which IGF-I activated NF-B and increased FLIP expression. When treated with IGF-I and LY294002, decreased NF-B DNA binding activity and increased expression of IB protein were detected in cultured thyroid cells, which further confirmed that NF-B was under the control of the PI3K pathway. Taken together, our results suggest that IGF-I regulates the expression of FLIP in FRTL cells by activating the PI3K/NF-B cascade.

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