Thyroid cancer is a prevalent endocrine malignancy around the world. Radioactive 131iodine (131I) 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 131I resistance of TC cells remains unclear. Here, we successfully established 131I-resistant TC cells and evaluated the impact of EGOT on 131I resistance in the cells. Our data showed that EGOT and PTEN expression was reduced but the miR-641 expression was enhanced in 131I-resistant TC cells. EGOT inhibited viability, induced apoptosis and enhanced DNA damage in 131I-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 131I resistance of TC cells in vitro. Thus, we conclude that lncRNA EGOT attenuated 131I 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.
Keywords: 131I resistance; PTEN; clinical functions; lncRNA EGOT; miR-641; thyroid cancer.