Long non-coding RNA EGOT is associated with iodine sensitivity and contributes to thyroid cancer progression by targeting miR-641/PTEN axis.

Thyroid cancer is a prevalent endocrine malignancy around the world. Radioactive iodine (I) therapy is widely applied in TC patients, but the resistance affects its effectiveness in the clinics. Long non-coding RNA (lncRNA) EGOT has been reported to induce an inhibitory effect on cancer progression, but the specific function of EGOT in I resistance of TC cells remains unclear. Here, we successfully established I-resistant TC cells and evaluated the impact of EGOT on I resistance in the cells. Our data showed that EGOT and PTEN expression was reduced but the miR-641 expression was enhanced in I-resistant TC cells. EGOT inhibited viability, induced apoptosis and enhanced DNA damage in I-resistant TC cells. Mechanically, we identified that EGOT induced PTEN expression by targeting miR-641 in 131I-resistant TC cells. Moreover, the depletion of PTEN and miR-641 mimic reversed EGOT-relieved I resistance of TC cells . Thus, we conclude that lncRNA EGOT attenuated I resistance of TC cells by targeting miR-641/PTEN axis. The clinical functions of EGOT in TC therapy deserve to be validated in future exploration.