Publication:
BPTF promotes glioma development through USP34-mediated de-ubiquitination of FOXC1

Simple item page
dc.contributor.authorPan, Yanling
dc.contributor.authorYuan, Feng
dc.contributor.authorLin, Zhiren
dc.contributor.authorLi, Yijie
dc.date.accessioned2025-01-16T09:57:02Z
dc.date.available2025-01-16T09:57:02Z
dc.date.issued2025
dc.description.abstractGlioma is the most prevalent malignant tumor of the brain, and the study of the molecular mechanisms associated with its development has important clinical significance. Our previous study found that BPTF promotes the malignant phenotype of glioma and is significantly associated with poor prognosis; the downstream regulatory mechanisms are explored in this study. Western blot and immuno-histochemical staining were used to detect protein expression in cells or tissues. BPTF knockdown as well as FOXC1-overexpressing lentiviruses were used in combination for the construction of the U251 cell model, leading to functional rescue experiments. CCK8 assay, flow cytometry, scratch assay, and Transwell assay were used to detect cell proliferation, apoptosis, and migration, respectively. Finally, immuno-precipitation assays, combined with western blot (WB), were used to detect the interaction between proteins as well as the level of ubiquitination modification. The obtained results suggested that BPTF knockdown may inhibit the malignant behavior of glioma cells by downregulating FOXC1 expression. Moreover, FOXC1 expression was significantly higher in glioma tissues than in normal brain tissues and was significantly associated with higher tumor stage and worse patient prognosis. Finally, the mechanism of FOXC1 regulation by BPTF was found to result from the affected protein stability of FOXC1 through USP34-mediated de-ubiquitylation. In conclusion, the BPTF/FOXC1 axis was identified as a key promotor in glioma development and may be a potential target in the inhibition of glioma development.es
dc.formatapplication/pdfes
dc.format.extent10es
dc.identifier.citationHistology and Histopathology Vol. 40, nº02 (2025)
dc.identifier.doihttps://doi.org/10.14670/HH-18-748
dc.identifier.issn0213-3911
dc.identifier.issn1699-5848
dc.identifier.urihttp://hdl.handle.net/10201/148582
dc.languageenges
dc.publisherUniversidad de Murcia, Departamento de Biologia Celular e Histiologiaes
dc.relationSin financiación externa a la Universidades
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectGliomaes
dc.subjectBPTFes
dc.subjectFOXC1es
dc.subjectUbiquitinationes
dc.subject.otherCDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncologíaes
dc.titleBPTF promotes glioma development through USP34-mediated de-ubiquitination of FOXC1es
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
Files
Original bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
Pan-40-205-214-2025.pdf
Size:
1.53 MB
Format:
Adobe Portable Document Format
Description:
Download
License bundle
Now showing 1 - 1 of 1
Thumbnail Image
Name:
license.txt
Size:
2.26 KB
Format:
Item-specific license agreed upon to submission
Description:
Download
Collections
Histology and histopathology Vol.40, nº2 (2025)