Regulatory role of estrogen-induced reactive oxygen species in the modulatory function of UCP 2 in papillary thyroid cancer cells.

Oxidative stress is postulated as one of the mechanisms underlying the estrogen's carcinogenic effect in thyroid cancer. But the fundamental mechanisms behind this carcinogenic effect remain elusive. Physiologically attainable concentrations of estrogen or estrogen metabolites have been made known to cause reactive oxygen species (ROS). It is envisioned that estrogen-induced ROS mediated signaling is a key congruent mechanism that drives the modulation of uncoupled proteins in papillary thyroid carcinoma cells. The present study investigates that estrogens may increase mitochondrial ROS production by repressing uncoupling proteins, which offers a new perspective on the understanding of why thyroid cancer occurs three times more often in females than in males, and the occurrence decreases after menopause.