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.