Tang Jin, Huang Xiao-Xia
Department of Clinical Laboratory, Hanzhong Central Hospital, Hanzhong 723000, Shaanxi, China.
Heliyon. 2023 Sep 1;9(9):e19713. doi: 10.1016/j.heliyon.2023.e19713. eCollection 2023 Sep.
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 . Different 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.
先前的研究表明，长链非编码RNA SNHG3与多种人类癌症有关，提示其致癌作用。然而，其在甲状腺癌中的具体作用及潜在分子机制仍不清楚。因此，本研究旨在阐明SNHG3在人类甲状腺癌中的作用及其与miR-339-5p/GPR62轴的相互作用。了解这些机制可为甲状腺癌的潜在治疗靶点提供见解。结果显示，SNHG3在人类甲状腺癌组织和细胞系中显著上调。敲低SNHG3可显著抑制CUTC5和IHH-4甲状腺癌细胞的增殖、迁移和侵袭。敲低SNHG3可诱导CUTC5和IHH-4细胞凋亡，并抑制异种移植肿瘤的生长。不同实验揭示了甲状腺癌细胞中SNHG3与微小RNA-339-5p（miR-339-5p）的相互作用。miR-339-5p在甲状腺癌组织和细胞系中的表达显著下调。然而，敲低SNHG3导致miR-339-5p显著上调。有趣的是，miR-339-5p的过表达通过对GPR62的转录后抑制在CUTC5和IHH-4细胞中发挥肿瘤抑制作用。敲低GPR62可显著抑制CUTC5和IHH-4细胞的增殖、迁移和侵袭。尽管如此，抑制miR-339-5p或过表达GPR62可避免SNHG3敲低对CUTC5和IHH-4细胞的生长抑制作用。结果表明，SNHG3通过miR-339-5p/GPR62轴在甲状腺癌中发挥致癌分子功能，可能成为其治疗靶点。
