Elucidation of the BMI1 interactome identifies novel regulatory roles in glioblastoma

Freire-Benéitez, Verónica; Pomella, Nicola; Millner, Thomas O; Dumas, Anaëlle; Niklison-Chirou, Maria Victoria; Maniati, Eleni; Wang, Jun; Rajeeve, Vinothini; Cutillas, Pedro R.; Marino, Silvia

doi:10.1093/narcan/zcab009

Cited by 4 publications

(2 citation statements)

References 118 publications

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“…Recently, Nayak ( 26 ) reported that nuclear VAV3 served an important role in B-cell lymphoblastic leukemogenesis through regulation of nuclear Bmi1 phosphorylation and polycomb repression complex-1 (PRC1) activity. the role of BMI 1 in the regulation of glioblastoma migration, invasion and stem cell renewal has been reported by numerous previous studies ( 27 – 30 ). Therefore, VAV3 could regulate glioblastoma migration, invasion and stem cell stemness via regulation of the PI3K-AKT signaling pathway or PRC1 activity.…”

Section: Discussionsupporting

confidence: 60%

VAV3 regulates glioblastoma cell proliferation, migration, invasion and cancer stem‑like cell self‑renewal

et al. 2023

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Glioblastoma multiforme (GBM; World Health Organization grade IV) is one of the most common and aggressive malignant brain tumors and has no effective treatment. Therefore, elucidation of the molecular mechanism of glioma development is very important for finding new therapeutic strategies. The present study evaluated the expression level of Vav guanine nucleotide exchange factor 3 (VAV3) using bioinformatics analysis and demonstrated that VAV3 was overexpressed in human glioblastoma and associated with patient survival. Knock down of VAV3 using shRNA in glioblastoma cells significantly inhibited glioblastoma cell migration, invasion and proliferation. Furthermore, downregulation of VAV3 expression inhibited the stem cell self-renewal capacity and decreased the expression levels of the stem cell markers Nestin and Sox2. Bioinformatic analysis demonstrated that VAV3 was a target gene of miR-218. Furthermore, overexpression of VAV3 markedly reversed the tumor suppressor effect of miR-218 in glioblastoma cell. These findings suggested that VAV3 could be a potential biomarker and therapeutic target for glioblastoma.

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Section: Discussionsupporting

confidence: 60%

VAV3 regulates glioblastoma cell proliferation, migration, invasion and cancer stem‑like cell self‑renewal

et al. 2023

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“…Consistent with these findings, iSREs accumulate large amounts of cholesterol, which is localized not only in the cell membrane associated with increased lipid rafts but also in an extensive network of lipid droplets. BMI1 has previously been implicated in regulating cholesterol homeostasis in glioblastoma cells, however, in these tumor cells BMI1 was considered to be a negative regulator of cholesterol synthesis via an indirect and undefined pathway (Freire-Beneitez, 2021). In contrast, BMI1 appears to act in iSREs as a positive regulator of cholesterol biosynthesis.…”

Section: Discussionmentioning

confidence: 99%

BMI1 regulates human erythroid self-renewal through both gene repression and gene activation

McGrath,

Koniski,

Murphy

et al. 2024

Preprint

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The limited proliferative capacity of erythroid precursors is a major obstacle to generate sufficient numbers of in vitro-derived red blood cells (RBC) for clinical purposes. We and others have determined that BMI1, a member of the polycomb repressive complex 1 (PRC1), is both necessary and sufficient to drive extensive proliferation of self-renewing erythroblasts (SREs). However, the mechanisms of BMI1 action remain poorly understood. BMI1 overexpression led to 10 billion-fold increase BMI1-induced (i)SRE self-renewal. Despite prolonged culture and BMI1 overexpression, human iSREs can terminally mature and agglutinate with typing reagent monoclonal antibodies against conventional RBC antigens. BMI1 and RING1B occupancy, along with repressive histone marks, were identified at known BMI1 target genes, including the INK-ARF locus, consistent with an altered cell cycle following BMI1 inhibition. We also identified upregulated BMI1 target genes with low repressive histone modifications, including key regulator of cholesterol homeostasis. Functional studies suggest that both cholesterol import and synthesis are essential for BMI1-associated self-renewal. These findings support the hypothesis that BMI1 regulates erythroid self-renewal not only through gene repression but also through gene activation and offer a strategy to expand the pool of immature erythroid precursors for eventual clinical uses.

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Recent Advances in Molecular and Cellular Functions of S100A10

Okura,

Bharadwaj,

Waisman

2023

Biomolecules

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S100A10 (p11, annexin II light chain, calpactin light chain) is a multifunctional protein with a wide range of physiological activity. S100A10 is unique among the S100 family members of proteins since it does not bind to Ca2+, despite its sequence and structural similarity. This review focuses on studies highlighting the structure, regulation, and binding partners of S100A10. The binding partners of S100A10 were collated and summarized.

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Elucidation of the BMI1 interactome identifies novel regulatory roles in glioblastoma

Cited by 4 publications

References 118 publications

VAV3 regulates glioblastoma cell proliferation, migration, invasion and cancer stem‑like cell self‑renewal

VAV3 regulates glioblastoma cell proliferation, migration, invasion and cancer stem‑like cell self‑renewal

BMI1 regulates human erythroid self-renewal through both gene repression and gene activation

Recent Advances in Molecular and Cellular Functions of S100A10

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