Circular RNA circKIF2A Contributes to the Progression of Neuroblastoma Through Regulating PRPS1 Expression by Sponging miR-377-3p
Biochemical Genetics, ISSN: 1573-4927, Vol: 60, Issue: 4, Page: 1380-1401
2022
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Most Recent News
Studies from Department of Pediatrics Have Provided New Information about Neuroblastomas (Circular Rna Circkif2a Contributes To the Progression of Neuroblastoma Through Regulating Prps1 Expression By Sponging Mir-377-3p)
2023 OCT 20 (NewsRx) -- By a News Reporter-Staff News Editor at Clinical Oncology Daily -- Investigators discuss new findings in Oncology - Neuroblastomas. According
Article Description
Neuroblastoma is a malignant tumor originating from the primitive neural crest. Circular RNA (circRNA) Kinesin Superfamily Protein 2A (circKIF2A, also known as hsa_circ_0129276) has been reported to be upregulated in neuroblastoma. However, the molecular mechanism of circKIF2A participated in neuroblastoma is poorly defined. We analyzed the expression levels of circKIF2A, microRNA-377-3p (miR-377-3p), and phosphoribosyl pyrophosphate synthetase 1 (PRPS1) in neuroblastoma tissues and cell lines (SK-N-AS and LAN-6) and explored their roles. The expression levels of CircKIF2A and PRPS1 were increased and that of miR-377-3p were decreased in 21 neuroblastoma tissues and cells. Functionally, the silencing of circKIF2A inhibited cell proliferation, migration, invasion, and glycolysis, boosted apoptosis in neuroblastoma cells in vitro, and blocked the growth of subcutaneously transplanted tumors in nude mice. Mechanically, circKIF2A could work as a sponge of miR-377-3p to enhance PRPS1 expression. CircKIF2A knockdown impedes cell proliferation, metastasis, and glycolysis partly by regulating the miR-377-3p/PRPS1 axis, suggesting that targeting circKIF2A can be a feasible therapeutic strategy for neuroblastoma.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85123018739&origin=inward; http://dx.doi.org/10.1007/s10528-021-10174-4; http://www.ncbi.nlm.nih.gov/pubmed/35039981; https://link.springer.com/10.1007/s10528-021-10174-4; https://dx.doi.org/10.1007/s10528-021-10174-4; https://link.springer.com/article/10.1007/s10528-021-10174-4
Springer Science and Business Media LLC
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