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Far upstream element-binding protein 1 regulates LSD1 alternative splicing to promote terminal differentiation of neural progenitors

ABSTRACT: Analysis of mouse neural progenitors with non targeting or FUBP1 targeting shRNA in proliferation and differentiation conditions

ORGANISM(S): Mus musculus

PROVIDER: GSE108537 | GEO | 2018/04/09

REPOSITORIES: GEO

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Far Upstream Element-Binding Protein 1 Regulates LSD1 Alternative Splicing to Promote Terminal Differentiation of Neural Progenitors.

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Far upstream element-binding protein 1 confers lobaplatin resistance via facilitating the arachidonic acid signaling in osteosarcoma

Project description:Purpose: To understand the mechanism of lobaplatin resistance and explore effective strategies for patients with osteosarcoma. Results: The expression of FUBP1 was remarkably elevated in osteosarcoma cell lines and clinical specimens compared with osteoblast cells and the normal bone. High expression of FUBP1 correlated with more aggressive phenotype and poor prognosis in osteosarcoma patients. Overexpression of FUBP1 confers lobaplatin resistance while inhibition of FUBP1 sensitizes osteosarcoma to lobaplatin cytotoxicity both in vivo and in vitro. Additionally, FUBP1 could regulate the transcription of PTGES, and subsequently activated the arachidonic acid signaling pathway in osteosarcoma cells treated with lobaplatin. Conclusions: Our investigation provided evidence that FUBP1 represents a potential therapeutic target for patients suffering from osteosarcoma. Targeting FUBP1 and its downstream AA signaling pathway may be a promising strategy to sensitize lobaplatin treatment during osteosarcoma chemoresistance. Methods: The expression of Far upstream element-binding protein 1(FUBP1) in human osteosarcoma cell lines and patient specimens were determined using Western blotting and Real-time PCR, respectively. 61 human osteosarcoma tissue specimens were analyzed using IHC to investigate the association between the expression of FUBP1 and the clinicopathological data of osteosarcoma patients. CCK8, FACS, clone formation assay, and in vivo animal xenograft model were used to determine the role of FUBP1 in lobaplatin-treating osteosarcoma. ChIP-seq and RNA-seq were performed, and the intersection genes and the enriched signaling pathways were analyzed. Luciferase assay and truncation assay were used to investigate the mechanism of FUBP1 promoting chemoresistance in osteosarcoma.

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