ArticleOncogene2021
The interactions of Bcl9/Bcl9L with β-catenin and Pygopus promote breast cancer growth, invasion, and metastasis.
Article in Oncogene, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Variants in the DDX6-CXCR5 autoimmune disease risk locus influence the regulatory network in immune cells and salivary gland.Annals of the rheumatic diseases · 2025Pooled it
- Targeting BCL9/BCL9L enhances CD4Acta pharmacologica Sinica · 2026Article
- Determination of copy number variations and affected gene networks in breast cancer.Biomedical reports · 2026Article
- Long-term cytokine exposure remodels the methylome and transcriptome of recessive dystrophic epidermolysis bullosa keratinocytes - a bioinformatic analysis.Frontiers in cell and developmental biology · 2026Article
- BCL9 as a Key Player in Wnt/β-catenin Signaling: Implications for Osteogenesis, Tissue Repair, and Oncology.Applied biochemistry and biotechnology · 2026Review
- Activated PLK1 promotes the migration and invasion of polyploid giant cancer cells with daughter cells via β-catenin/STAT3 signaling pathway.Human cell · 2025Article
- The developmental factor TBX3 engages with the Wnt/β-catenin transcriptional complex in colorectal cancer to regulate metastasis genes.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Molecular Characteristics of Prognosis and Chemotherapy Response in Breast Cancer: Biomarker Identification Based on Gene Mutations and Pathway.Journal of breast cancer · 2025Article
- Disrupting β-Catenin/BCL9 interaction with a peptide prodrug boosts immunotherapy in colorectal cancer.Frontiers in immunology · 2025Article
- Frizzled receptors: gatekeepers of Wnt signaling in development and disease.Frontiers in cell and developmental biology · 2025Review
- Analyzing the Impact of the Highest Expressed Epstein-Barr Virus-Encoded microRNAs on the Host Cell Transcriptome.International journal of molecular sciences · 2024Article
- Targeting BCL9/BCL9L enhances antigen presentation by promoting conventional type 1 dendritic cell (cDC1) activation and tumor infiltration.Signal transduction and targeted therapy · 2024Article
- Article
- Ezh2 promotes mammary tumor initiation through epigenetic regulation of the Wnt and mTORC1 signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Potential role of PIM1 inhibition in the treatment of SARS-CoV-2 infection.Journal, genetic engineering & biotechnology · 2023Article
- Transcriptome analysis reveals molecular mechanisms of lymphocystis formation caused by lymphocystis disease virus infection in flounder (Frontiers in immunology · 2023Article
- PLK1-mediated phosphorylation of β-catenin enhances its stability and transcriptional activity for extracellular matrix remodeling in metastatic NSCLC.Theranostics · 2023Article
- Article
- Nuclear Expression of Pygo2 Correlates with Poorly Differentiated State Involving c-Myc, PCNA and Bcl9 in Myanmar Hepatocellular Carcinoma.Acta histochemica et cytochemica · 2021Article
- Characteristics of genomic mutations and signaling pathway alterations in thymic epithelial tumors.Annals of translational medicine · 2021Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Canonical Wnt/β-catenin signaling is an established regulator of cellular state and its critical contributions to tumor initiation, malignant tumor progression and metastasis formation have been demonstrated in various cancer types. Here, we investigated how the binding of β-catenin to the transcriptional coactivators B-cell CLL/lymphoma 9 (Bcl9) and Bcl9-Like (Bcl9L) affected mammary gland carcinogenesis in the MMTV-PyMT transgenic mouse model of metastatic breast cancer. Conditional knockout of both Bcl9 and Bcl9L resulted into tumor cell death. In contrast, disrupting the interaction of Bcl9/Bcl9L with β-catenin, either by deletion of their HD2 domains or by a point mutation in the N-terminal domain of β-catenin (D164A), diminished primary tumor growth and tumor cell proliferation and reduced tumor cell invasion and lung metastasis. In comparison, the disruption of HD1 domain-mediated binding of Bcl9/Bcl9L to Pygopus had only moderate effects. Interestingly, interfering with the β-catenin-Bcl9/Bcl9L-Pygo chain of adapters only partially impaired the transcriptional response of mammary tumor cells to Wnt3a and TGFβ treatments. Together, the results indicate that Bcl9/Bcl9L modulate but are not critically required for canonical Wnt signaling in its contribution to breast cancer growth and malignant progression, a notion consistent with the "just-right" hypothesis of Wnt-driven tumor progression.
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