Hsa_circ_0001480 affects osteosarcoma progression by regulating the miR‐363‐3p/IBSP pathway

Osteosarcoma (OS) is a malignant bone tumor that commonly affects young individuals. Circular RNAs (circRNAs) are associated with OS progression. In this study, we aimed to determine the role of hsa_circ_0001480 (circ_0001480) in OS development. OS cell invasion, viability, and colony numbers were a...

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Veröffentlicht in:Biotechnology and applied biochemistry 2024-08, Vol.71 (4), p.721-732
Hauptverfasser: Bi, Guijuan, Zhang, Li
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Sprache:eng
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Zusammenfassung:Osteosarcoma (OS) is a malignant bone tumor that commonly affects young individuals. Circular RNAs (circRNAs) are associated with OS progression. In this study, we aimed to determine the role of hsa_circ_0001480 (circ_0001480) in OS development. OS cell invasion, viability, and colony numbers were assessed via transwell, cell counting kit‐8, and colony formation assays, respectively. Tumor growth in vivo was also assessed using an OS mouse model. Additionally, targeted associations among the integrin‐binding sialoprotein (IBSP), microRNA (miR)‐363‐3p, and circ_0001480 were evaluated via RNA immunoprecipitation and dual luciferase reporter assays, whereas their expression levels in OS cells and tissues were determined via quantitative reverse transcription‐polymerase chain reaction and western blotting. Loss of circ_0001480 or IBSP significantly inhibited the proliferation and invasion of OS cells, but this effect was reversed by miR‐363‐3p downregulation. Moreover, circ_0001480 knockdown inhibited neoplasm growth in vivo. circ_0001480 directly bound to miR‐363‐3p, which further modulated IBSP. Both circ_0001480 and IBSP levels were high, whereas miR‐363‐3p levels were low in OS cells. Furthermore, low miR‐363‐3p levels attenuated the suppressive effects of circ_0001480 silencing on the proliferation and invasion of OS cells; however, loss of IBSP partially reversed these effects. Overall, our findings revealed circ_0001480 an oncogenic circRNA stimulating OS progression by modulating the miR‐363‐3p/IBSP pathway, suggesting its potential for OS treatment.
ISSN:0885-4513
1470-8744
1470-8744
DOI:10.1002/bab.2571