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Submitted on September 19, 2003
Accepted on February 9, 2004
Third Department of Internal Medicine, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan
* To whom correspondence should be addressed. E-mail: tetsurou{at}yamanashi.ac.jp.
Iodide uptake by the thyroid is mediated by the sodium/iodide symporter (NIS). Upon iodide uptake, thyroperoxidase (TPO) catalyzes iodination of tyrosine residues in thyroglobulin (Tg), retaining iodide within thyroid follicles. Dedifferentiation-induced loss of these functions in cancers, renders them unresponsive to radioiodide, occurs with most poorly differentiated and anaplastic tumors. We focused on the histone deacetylase inhibitors (HDACI) as a way to induce differentiation of thyroid cancer cells. We assessed re-expression of thyroid-specific genes mRNA induced by HDACI using quantitative RT-PCR and immunostaining in poorly differentiated papillary and anaplastic thyroid cancer cells. HDACI induced expression of thyroid-specific genes mRNAs and proteins, and accumulation of radioiodide through iodination of generic cellular proteins were detected. HDACI-treated tumors could specifically accumulate 125I as revealed by imaging experiments and radioiodide concentration in vivo. In an attempt to determine the mechanism of these gene expression occurred, we detected the inhibition of protein synthesis by cycloheximide led to up-regulate the expression of TPO and Tg mRNA in HDACI-treated cells, and down-regulated that of NIS mRNA. Together, our results suggest that HDACI-induced expression of thyroid-specific genes, some of which is mediated by some protein synthesis, may contribute for development of novel strategy against thyroid cancer.
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