ArticleBlood advances2021
Frequent mutations of FBXO11 highlight BCL6 as a therapeutic target in Burkitt lymphoma.
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- The Growth Supporting Role of ZDHHC11 Is Linked to the MEF2B-BCL6 Regulatory Circuit in Burkitt Lymphoma.International journal of cancer · 2026Article
- Pleiotropic Roles of FBXO11 in Tumorigenesis: Implications for Targeted Therapy.Cancer science · 2026Review
- Burkitt Lymphoma-A Guide to Biological Features, Diagnosis and Differential Diagnosis.Cancers · 2026Review
- Multi-omic analysis identifies a multi-step pathology in a case of multiple chorangioma syndrome in monochorionic twins.Orphanet journal of rare diseases · 2026Article
- FBXO11 suppression rewires an NPM1-centered interactome influencing the progression of myelodysplastic syndrome.The Journal of clinical investigation · 2026Article
- F-box proteins in cancer: from cancer cells to the tumor microenvironment.Cell communication and signaling : CCS · 2025Review
- Proteasomal activation ameliorates neuronal phenotypes linked to FBXO11-deficiency.HGG advances · 2025Article
- The FBXO45-GEF-H1 Axis Controls Germinal Center Formation and B-cell Lymphomagenesis.Cancer discovery · 2025Article
- The F-box E3 ligase protein FBXO11 regulates EBNA3C-associated degradation of BCL6.Journal of virology · 2024Article
- ALK inhibitors increase ALK expression and sensitize neuroblastoma cells to ALK.CAR-T cells.Cancer cell · 2023Article
- Inhibitors Targeting the F-BOX Proteins.Cell biochemistry and biophysics · 2023Review
- Targeting MYC-driven lymphoma: lessons learned and future directions.Cancer drug resistance (Alhambra, Calif.) · 2023Review
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Authors and funding
26 authors at 11 institutions in 5 countries.
Funding
Abstract
The expression of BCL6 in B-cell lymphoma can be deregulated by chromosomal translocations, somatic mutations in the promoter regulatory regions, or reduced proteasome-mediated degradation. FBXO11 was recently identified as a ubiquitin ligase that is involved in the degradation of BCL6, and it is frequently inactivated in lymphoma or other tumors. Here, we show that FBXO11 mutations are found in 23% of patients with Burkitt lymphoma (BL). FBXO11 mutations impaired BCL6 degradation, and the deletion of FBXO11 protein completely stabilized BCL6 levels in human BL cell lines. Conditional deletion of 1 or 2 copies of the FBXO11 gene in mice cooperated with oncogenic MYC and accelerated B-cell lymphoma onset, providing experimental evidence that FBXO11 is a haploinsufficient oncosuppressor in B-cell lymphoma. In wild-type and FBXO11-deficient BL mouse and human cell lines, targeting BCL6 via specific degraders or inhibitors partially impaired lymphoma growth in vitro and in vivo. Inhibition of MYC by the Omomyc mini-protein blocked cell proliferation and increased apoptosis, effects further increased by combined BCL6 targeting. Thus, by validating the functional role of FBXO11 mutations in BL, we further highlight the key role of BCL6 in BL biology and provide evidence that innovative therapeutic approaches, such as BCL6 degraders and direct MYC inhibition, could be exploited as a targeted therapy for BL.
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