Abstract
Previous studies have implicated SNHG3, a long non-coding RNA, in various human cancers, suggesting its oncogenic role. However, its specific involvement in thyroid cancer and the underlying molecular mechanisms remain unclear. Therefore, this study aims to elucidate the role of SNHG3 in human thyroid cancer and its interaction with the miR-339-5p/GPR62 axis. Understanding these mechanisms could provide insights into potential therapeutic targets for managing thyroid cancer. Results revealed significant upregulation of SNHG3 in human thyroid cancer tissues and cell lines. Knockdown of SNHG3 significantly suppressed proliferation, migration and invasion of CUTC5 and IHH-4 thyroid cancer cells. Knockdown of SNHG3 induces apoptosis in CUTC5 and IHH-4 cells and also inhibits the growth of xenografted tumors in vivo. Different in vitro assays revealed the interaction of SNHG3 with microRNA-339-5p (miR-339-5p) in thyroid cancer cells. Expression of miR-339-5p was significantly downregulated in thyroid cancer tissues and cell lines. However, the knockdown of SNHG3 caused significant upregulation of miR-339-5p. Interestingly, overexpression of miR-339-5p exerted tumor-suppressive effects in CUTC5 and IHH-4 cells via post-transcriptional suppression of GPR62. Knockdown of GPR62 significantly inhibited the proliferation, migration and invasion of CUTC5 and IHH-4 cells. Nonetheless, inhibition of miR-339-5p or overexpression of GPR62 avoids the growth inhibitory effects of SNHG3 knockdown in CUTC5 and IHH-4 cells. Results indicated that SNHG3 exerts oncogenic molecular function in thyroid cancer via miR-339-5p/GPR62 axis and may act as a therapeutic target for its management.