Abstract
Epidemiological studies suggest an important link between obesity and thyroid cancer. The adipose tissue-derived polypeptide leptin acting via leptin receptor may modulate cell migration of thyroid cancer cells. Previously we have demonstrated that leptin receptor is overexpressed in papillary thyroid cancer and is associated with tumor aggressiveness. The present study was undertaken to explore the possible regulatory factors which would influence leptin receptor expression in papillary thyroid cancer cells. We found that DNA methyltransferase inhibitor (5-Aza-2′-deoxycytidine) and histone deacetylase inhibitor (trichostatin A) reduced leptin receptor expression. Conversely, insulin upregulated leptin receptor expression in a time- and dose-dependent manner. Hypoxia-mimicking agent (cobalt chloride) had no effect on leptin receptor expression. Taken together, our study provides evidence that epigenetic events and insulin stimulation take part in regulation of leptin receptor expression in papillary thyroid cancer cells.
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