ArticleCellular oncology (Dordrecht, Netherlands)2020
BRCA1-associated protein inhibits glioma cell proliferation and migration and glioma stem cell self-renewal via the TGF-β/PI3K/AKT/mTOR signalling pathway.
Article in Cellular oncology (Dordrecht, Netherlands), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 38 citations in OpenAlex.
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- The Comprehensive Analysis of m6A-Associated Anoikis Genes in Low-Grade Gliomas.Brain sciences · 2023Article
- Genome-wide identification and phenotypic characterization of seizure-associated copy number variations in 741,075 individuals.Nature communications · 2023Article
- Circadian Period 2 (Per2) downregulate inhibitor of differentiation 3 (Id3) expression via PTEN/AKT/Smad5 axis to inhibits glioma cell proliferation.Bioengineered · 2022Article
- Article
- BRAP2 inhibits the Ras/Raf/MEK and PI3K/Akt pathways in leukemia cells, thereby inducing apoptosis and inhibiting cell growth.Experimental and therapeutic medicine · 2021Article
- MARCH6 promotes Papillary Thyroid Cancer development by destabilizing DHX9.International journal of biological sciences · 2021Article
- MiR-4310 induced by SP1 targets PTEN to promote glioma progression.Cancer cell international · 2020Article
- MNAT1 promotes proliferation and the chemo-resistance of osteosarcoma cell to cisplatin through regulating PI3K/Akt/mTOR pathway.BMC cancer · 2020Article
- Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review.Frontiers in pharmacology · 2020Review
- LncRNA MALAT1 Regulates the Cell Proliferation and Cisplatin Resistance in Gastric Cancer via PI3K/AKT Pathway.Cancer management and research · 2020Article
- CBX2 Induces Glioma Cell Proliferation and Invasion Through the Akt/PI3K Pathway.Technology in cancer research & treatmentArticle
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
Abstract
purposeBRCA1-associated protein (BRAP) was first identified by its ability to bind to the nuclear localization signalling motif of BRCA1 and other proteins. Subsequently, human BRAP has been found to exert multiple functions, many of which are related to cancer development. Up till now, however, the role of BRAP in glioma development has remained obscure. Here, we report a role for BRAP in mediating the proliferation and migration of glioma cells both in vitro and in vivo.
methodsThe expression of BRAP in 98 glioma patient samples was determined by immunohistochemistry, after which associations between BRAP expression and patient prognosis were assessed. A short hairpin RNA (shRNA) was used to knock down BRAP and an expression vector was used to exogenously overexpress BRAP in glioma cells. The effects of BRAP expression on tumour cell behaviour in vitro and in an in vivo xenograft mouse model were examined.
resultsWe found that in glioma patients BRAP expression was associated with a favourable prognosis. We also found that shRNA-mediated knockdown of BRAP facilitated the proliferation and migration of glioma cells and the self-renewal of glioma stem cells. In parallel, we found that BRAP knockdown increased tumour growth and invasion and decreased survival in an in vivo glioma xenograft mouse model. Mechanistically, we found that BRAP inhibited glioma cell proliferation and migration, as well as glioma stem cell self-renewal via the TGF-β/PI3K/AKT/mTOR signalling pathway.
conclusionsTogether, our findings identify BRAP as a mediator of glioma cell proliferation, migration and glioma stem cell self-renewal.
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