CircRNA casein kinase 1 gamma 1 (circ‐CSNK1G1) plays carcinogenic effects in thyroid cancer by acting as miR‐149‐5p sponge and relieving the suppression of miR‐149‐5p on mitogen‐activated protein kinase 1 (MAPK1)

Background The initiation and development of thyroid cancer may be associated with the deregulation of circular RNAs (circRNAs). The purpose of this work was to explore the role of circRNA casein kinase 1 gamma 1 (circ‐CSNK1G1) in thyroid cancer. Methods The expression of circ‐CSNK1G1, miR‐149‐5p, and mitogen‐activated protein kinase 1 (MAPK1) was concluded using quantitative real‐time PCR (qPCR), and the expression of MAPK1 protein was detected by Western blot assay. Cell viability was monitored by CCK‐8 assay. Cell proliferation was determined by colony formation assay and EdU assay. Cell apoptosis and cycle were checked by flow cytometry assay. Cell invasion was determined by transwell assay. The predicted binding relationship between miR‐149‐5p and circ‐CSNK1G1 or MAPK1 was verified by dual‐luciferase reporter assay. The role of circ‐CSNK1G1 in vivo was determined by establishing animal models. Results The present work discovered the upregulation of circ‐CSNK1G1 in tumor tissues of thyroid cancer. In function, circ‐CSNK1G1 knockdown inhibited proliferation, survival, and invasion in cancer cells, and tumor growth in mouse models. MiR‐149‐5p was a target of circ‐CSNK1G1, and the anti‐tumor effects of circ‐CSNK1G1 knockdown were abolished by miR‐149‐5p downregulation. In addition, miR‐149‐5p directly targeted MAPK1, and miR‐149‐5p restoration‐inhibited cell proliferation and invasion were recovered by MAPK1 overexpression. Conclusion Circ‐CSNK1G1 acted as miR‐149‐5p to relieve the inhibition of miR‐149‐5p on MAPK1, thus promoting the malignant development of thyroid cancer.