Hsa_circ_0023990 promotes tumor growth and glycolysis in dedifferentiated TC via targeting miR-485-5p/FOXM1 axis

xlomafota13 shared this article with you from Inoreader Hsa_circ_0023990 promotes tumor growth and glycolysis in dedifferentiated TC via targeting miR-485-5p/FOXM1 axis Via radioactive iodine Endocrinology. 2021 Aug 20:bqab172. doi: 10.1210/endocr/bqab172. Online ahead of print. ABSTRACT BACKGROUND: During the transformation to dedifferentiated TC types, the ability of papillary thyroid carcinomas (PTC) to concentrate radioactive iodine might be lost, raising difficulty for the current therapy. Circular RNAs (circRNAs) were proved to be implicated in the progression of various cancers. In this study, we aimed to investigate the functional role and mechanism of hsa_circ_0 023990 in dedifferentiated TC. METHODS: The expression pattern of genes were detected utilizing qPCR or western blot assays. Cell proliferation was determined by CCK8, colony formation, EdU and cell cycle assays. Glycolysis was assessed using glucose uptake and lactate production assays. Luciferase reporter assay was performed to examine the interactions between miR-485-5p and hsa_circ_0023990 or FOXM1. Xenograft assay was allowed for observation of tumor growth in vivo. RESULTS: Hsa_circ_0023990 and FOXM1 were upregulated in dedifferentiated TC tissues and cell lines. The higher level of hsa_circ_0023900 could stimulate the proliferation and glycolysis of dedifferentiated TC cells via positively regulating FOXM1. Mechanistically, miR-485-5p was demonstrated to interact with hsa_circ_0023990 and FOXM1 and involved in the regulation of has_circ_0023990 and FOXM1 in TC biological processes. CONCLUSION: Our results discovered the functional network of hsa_circ_0023990 in dedifferentiated TC development by facilitating cell proliferation and glycolysis via miR-485-5p/FOXM1 axis, implying that hsa_circ_0023990 might be a potential therapeutic target for the dedifferentiated TC treatment. PMID:34414414 | DOI:10.1210/endocr/bqab172 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.