ArticleNucleic acids research2024
The function of BCL11B in base excision repair contributes to its dual role as an oncogene and a haplo-insufficient tumor suppressor gene.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- BCL11B predetermines a persister state in breast cancer that is reversed by TNFα.Science advances · 2026Article
- Circadian gene CLOCK-mediated LLPS of NBR1 and p62/SQSTM1 inhibits proliferation and migration of nasopharyngeal carcinoma.Cell death & disease · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- The transcription factor BCL11B drives NK cell cytotoxicity and antitumor activity.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The function of MYC in base excision repair protects against RAS-induced senescence.Nucleic acids research · 2025Article
- The efferocytosis process in aging: Supporting evidence, mechanisms, and therapeutic prospects for age-related diseases.Journal of advanced research · 2025Review
- Analysis of the Transcriptional Control ofAnimals : an open access journal from MDPI · 2025Article
- The BCL11A transcription factor stimulates the enzymatic activities of the OGG1 DNA glycosylase.Biological chemistry · 2024Article
- Dual role ofBlood science (Baltimore, Md.) · 2024Review
- Pivotal role of BCL11B in the immune, hematopoietic and nervous systems: a review of the BCL11B-associated phenotypes from the genetic perspective.Genes and immunity · 2024Review
- Multiomic analyses reveal new targets of polycomb repressor complex 2 in Schwann lineage cells and malignant peripheral nerve sheath tumors.Neuro-oncology advancesArticle
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Genetic studies in mice and human cancers established BCL11B as a haploinsufficient tumor suppressor gene. Paradoxically, BCL11B is overexpressed in some human cancers where its knockdown is synthetic lethal. We identified the BCL11B protein in a proximity-dependent biotinylation screen performed with the DNA glycosylase NTHL1. In vitro DNA repair assays demonstrated that both BCL11B and a small recombinant BCL11B213-560 protein lacking transcription regulation potential can stimulate the enzymatic activities of two base excision repair (BER) enzymes: NTHL1 and Pol β. In cells, BCL11B is rapidly recruited to sites of DNA damage caused by laser microirradiation. BCL11B knockdown delays, whereas ectopic expression of BCL11B213-560 accelerates, the repair of oxidative DNA damage. Inactivation of one BCL11B allele in TK6 lymphoblastoid cells causes an increase in spontaneous and radiation-induced mutation rates. In turn, ectopic expression of BCL11B213-560 cooperates with the RAS oncogene in cell transformation by reducing DNA damage and cellular senescence. These findings indicate that BCL11B functions as a BER accessory factor, safeguarding normal cells from acquiring mutations. Paradoxically, it also enables the survival of cancer cells that would otherwise undergo senescence or apoptosis due to oxidative DNA damage resulting from the elevated production of reactive oxygen species.
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Registered trials
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