LncRNA GAS5 sponges miR‐362‐5p to promote sensitivity of thyroid cancer cells to 131I by upregulating SMG1

This study aims to investigate the role of lncRNA growth arrest‐specific transcript 5 (GAS5)/miR‐362‐5p/suppressor of morphogenesis in the genitalia 1 (SMG1) axis in 131I‐resistance in thyroid cancer (TC). GAS5, miR‐362‐5p, and SMG1 expression in TC tissues was assessed and the 131I‐resistant TC cells were established, which were treated with altered GAS5, miR‐362‐5p, and SMG1. The proliferation and apoptosis of 131I‐resistant TC cells were detected, and the expression of Akt/mTOR signaling pathway‐related proteins was assessed. Binding relations between GAS5 and miR‐362‐5p, and miR‐362‐5p and SMG1 were confirmed. The role of GAS5 in 131I‐resistant TC cell growth in vivo was observed. GAS5 was downregulated and miR‐362‐5p was upregulated in TC tissues and 131I‐resistant cells. The 131I‐resistant TC cells had enhanced proliferation and repressed apoptosis, and the Akt/mTOR signaling pathway was activated. Overexpressed GAS5 strengthened 131I sensitivity and suppressed TC cell growth, while upregulated miR‐362‐5p had an opposite effect. MiR‐362‐5p upregulation reversed the effect of GAS5, and SMG1 overexpression eliminated the impact of miR‐362‐5p upregulation on 131I‐resistant TC cells. GAS5 competitively binds to miR‐362‐5p and SMG1 is targeted by miR‐362‐5p. GAS5 sponges miR‐362‐5p to promote sensitivity of TC cells to 131I by upregulating SMG1 and inactivating Akt/mTOR signaling pathway.