ArticleOncotarget2014
The BCL9-2 proto-oncogene governs estrogen receptor alpha expression in breast tumorigenesis.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Wnt/β-Catenin Signalling and Its Cofactor BCL9L Have an Oncogenic Effect in Bladder Cancer Cells.International journal of molecular sciences · 2022Article
- Somatic structural variant formation is guided by and influences genome architecture.Genome research · 2022Article
- The interactions of Bcl9/Bcl9L with β-catenin and Pygopus promote breast cancer growth, invasion, and metastasis.Oncogene · 2021Article
- BCL9/BCL9L promotes tumorigenicity through immune-dependent and independent mechanisms in triple negative breast cancer.Oncogene · 2021Article
- Bcl9 and Pygo synergise downstream of Apc to effect intestinal neoplasia in FAP mouse models.Nature communications · 2019Article
- Prioritizing predictive biomarkers for gene essentiality in cancer cells with mRNA expression data and DNA copy number profile.Bioinformatics (Oxford, England) · 2018Article
- The nuclear receptor ERβ engages AGO2 in regulation of gene transcription, RNA splicing and RISC loading.Genome biology · 2017Article
- miR-30a acts as a tumor suppressor by double-targeting COX-2 and BCL9 in H. pylori gastric cancer models.Scientific reports · 2017Article
- Tetrahelical structural family adopted by AGCGA-rich regulatory DNA regions.Nature communications · 2017Article
- Nerve growth factor modulates the tumor cells migration in ovarian cancer through the WNT/β-catenin pathway.Oncotarget · 2016Article
- The role of Pygo2 for Wnt/ß-catenin signaling activity during intestinal tumor initiation and progression.Oncotarget · 2016Article
- Role of BCL9L in transforming growth factor-β (TGF-β)-induced epithelial-to-mesenchymal-transition (EMT) and metastasis of pancreatic cancer.Oncotarget · 2016Article
- WDR5 high expression and its effect on tumorigenesis in leukemia.Oncotarget · 2016Article
- Expression profiling of in vivo ductal carcinoma in situ progression models identified B cell lymphoma-9 as a molecular driver of breast cancer invasion.Breast cancer research : BCR · 2015Article
- The structural basis for cancer treatment decisions.Oncotarget · 2014Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The majority of human breast cancers express estrogen receptor alpha (ER), which is important for therapy with anti-estrogens. Here we describe the role of BCL9-2, a proto-oncogene previously characterized as co-activator of Wnt/ß-catenin signaling, for mammary tumorigenesis in mice and human. ER positive human breast cancers showed overexpression of BCL9-2 and tamoxifen treated patients with high BCL9-2 demonstrated a better survival. BCL9-2 was upregulated during puberty and pregnancy in normal mammary epithelia, but downregulated in the involuted gland. BCL9-2 overexpression in vivo delayed the mammary involution and induced alveolar hyperplasia. Moreover, aged BCL9-2 transgenic mice developed ductal-like mammary tumors with high nuclear ER expression. We found, that primary cell cultures of BCL9-2 breast tumors responded to tamoxifen treatment. Moreover, BCL9-2 regulated the expression of ER and the proliferation of human breast cancer cells independently of ß-catenin. Finally, we describe a novel mechanism, how BCL9-2 regulates ER transcription by interaction with Sp1 through the proximal ESR1 gene promoter. In summary, BCL9-2 induces ER positive breast cancers in vivo, regulates ER expression by a novel ß-catenin independent mechanism in breast cancer cells, and might predict the therapy response to tamoxifen treatment.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.