lncRNA ZNF674-AS1 inhibits the migration, invasion and epithelial-mesenchymal transition of thyroid cancer cells by modulating the miR-181a/SOCS4 axis

• Published in: Molecular and cellular endocrinology 2022-03, Vol.544, p.111551-111551, Article 111551
• Main Authors: Le, Fei, Li, Hong-Mi, Lv, Qiao-Li, Chen, Jun-Jun, Lin, Qian-Xia, Ji, Yu-Long, Yi, Bo
• Format: Article
• Language: English
• Subjects: EMT; lncRNA ZNF674-AS1; miR-181a; SOCS4; Thyroid cancer
• ISSN: 0303-7207; 1872-8057
• DOI: 10.1016/j.mce.2021.111551

Thyroid cancer (TC) is a very common endocrine cancer worldwide. Further understanding and revealing the molecular mechanism underlying thyroid cancer are indispensable for the development of effective diagnosis and treatments. Long non-coding RNAs (lncRNAs), a series of non-coding RNAs with a length of >200 nts, have been regarded as crucial regulators of many cancers playing a tumor suppressive or oncogenic role, depending on circumstances. lncRNA ZNF674-AS1 was reported to be abnormally expressed in TC, but the exact mechanism remains unclear. This study aims to probe the mechanism and roles of ZNF674-AS1 in TC. The expression patterns of RNAs and proteins were determined via qRT–PCR and western blotting, respectively. Cell proliferation, migration and invasion were detected using MTT and Transwell assays. ZNF674-AS1 and SOCS4 expression were remarkably reduced while miR-181a was upregulated in TC tissues and cells. Enforced expression of ZNF674-AS1 inhibited proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro and reduced tumour growth in vivo. Mechanistic assays verified that ZNF674-AS1 directly interacted with miR-181a to increase SOCS4 expression. In addition, miR-181a overexpression aggravated proliferation, metastasis and EMT by inhibiting SOCS4. Interestingly, inhibition of miR-181a diminished the promoting effects of ZNF674-AS1 silencing on the malignant behaviours of TC cells. These data illustrated that ZNF674-AS1 alleviated TC progression by modulating the miR-181a/SOCS4 axis (graphical abstract), further suggesting that ZNF674-AS1 might be used as a therapheutic target in TC treatment. [Display omitted] •ZNF674-AS1 and SOCS4 were reduced but miR-181a was upregulated in TC.•Overexpression of ZNF674-AS1 suppressed the metastasis and EMT in TC cells.•ZNF674-AS1 worked as a ceRNAs to increase SOCS4 via sponging miR-181a.•ZNF674-AS1 overexpression suppressed TC progress by regulating miR-181a/SOCS4 axis.