Aging
Navigate
Submit an Article
Research Paper|Volume 15, Issue 22|pp 13542—13557

Long non-coding RNA EGOT is associated with 131iodine sensitivity and contributes to thyroid cancer progression by targeting miR-641/PTEN axis

Ming Wang1, Zhengchao Wei1, Shuang Wang2, Wenjuan Feng3, Lihua Shang4, Xiaosong Sun1
  • 1Department of Thyroid-Head and Neck Oncosurgery-1, Jilin Cancer Hospital, Changchun, Jilin Province, China
  • 2Department of Thoracic Oncosurgery-1, Jilin Cancer Hospital, Changchun, Jilin Province, China
  • 3Department of Gynecologic Oncosurgery-2, Jilin Cancer Hospital, Changchun, Jilin Province, China
  • 4Department of Breast Oncosurgery-2, Jilin Cancer Hospital, Changchun, Jilin Province, China
Received: May 4, 2021Accepted: February 15, 2022Published: November 21, 2023
https://doi.org/10.18632/aging.205284

Copyright: © 2023 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.