ArticleNature communications2021
A transcription-based mechanism for oncogenic β-catenin-induced lethality in BRCA1/2-deficient cells.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- KPNA2 knockdown suppresses gastric cancer progression through modulation of the β-catenin/EMT signaling axis, inducing cell cycle arrest, apoptosis, and reduced metastatic capacity.Journal of molecular histology · 2026Article
- Endogenous p21 levels protect genomic stability by suppressing both excess and restrained nascent DNA syntheses.Science advances · 2025Article
- TRIP13 protects pancreatic cancer cells against intrinsic and therapy-induced DNA replication stress.NAR cancer · 2025Article
- Transcription-Replication Conflicts as a Source of Genome Instability.Annual review of genetics · 2023Review
- Wnt3a signaling with serum supply induces replication stress in cultured cells.Biochemistry and biophysics reports · 2023Article
- Article
- Mitotic DNA synthesis is caused by transcription-replication conflicts in BRCA2-deficient cells.Molecular cell · 2022Article
- Fine-tuning of β-catenin in mouse thymic epithelial cells is required for postnatal T-cell development.eLife · 2022Article
- Identification of MAD2L1 as a Potential Biomarker in Hepatocellular Carcinoma via Comprehensive Bioinformatics Analysis.BioMed research international · 2022Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
Abstract
BRCA1 or BRCA2 germline mutations predispose to breast, ovarian and other cancers. High-throughput sequencing of tumour genomes revealed that oncogene amplification and BRCA1/2 mutations are mutually exclusive in cancer, however the molecular mechanism underlying this incompatibility remains unknown. Here, we report that activation of β-catenin, an oncogene of the WNT signalling pathway, inhibits proliferation of BRCA1/2-deficient cells. RNA-seq analyses revealed β-catenin-induced discrete transcriptome alterations in BRCA2-deficient cells, including suppression of CDKN1A gene encoding the CDK inhibitor p21. This accelerates G1/S transition, triggering illegitimate origin firing and DNA damage. In addition, β-catenin activation accelerates replication fork progression in BRCA2-deficient cells, which is critically dependent on p21 downregulation. Importantly, we find that upregulated p21 expression is essential for the survival of BRCA2-deficient cells and tumours. Thus, our work demonstrates that β-catenin toxicity in cancer cells with compromised BRCA1/2 function is driven by transcriptional alterations that cause aberrant replication and inflict DNA damage.
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Registered trials
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