ArticleBreast cancer research : BCR2015
Expression profiling of in vivo ductal carcinoma in situ progression models identified B cell lymphoma-9 as a molecular driver of breast cancer invasion.
Article in Breast cancer research : BCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 45 citations in OpenAlex.
- Racial Disparity in Ductal Carcinoma in Situ: Risk-Predictive and Actionable Biomarkers for Early Intervention.Cancers · 2026Review
- Genomic and transcriptomic analyses identify distinctive features of triple-negative inflammatory breast cancer.NPJ precision oncology · 2024Article
- How much do we know about the metastatic process?Clinical & experimental metastasis · 2024Review
- BCL9 is a Risk Factor of Neck Lymph Nodes Metastasis and Correlated with Immune Cell Infiltration in Papillary Thyroid Carcinoma.International journal of general medicine · 2024Article
- Human Ductal Carcinoma In Situ: Advances and Future Perspectives.Cold Spring Harbor perspectives in medicine · 2023Review
- MIND the translational gap: Preclinical models of ductal carcinoma in situ.Clinical and translational medicine · 2023Article
- New Biomarkers Based on Dendritic Cells for Breast Cancer Treatment and Prognosis Diagnosis.International journal of molecular sciences · 2023Article
- Wnt/β-catenin signaling pathway in the tumor progression of adrenocortical carcinoma.Frontiers in endocrinology · 2023Review
- Article
- New ZW4864 Derivatives as Small-Molecule Inhibitors for the β-Catenin/BCL9 Protein-Protein Interaction.ACS medicinal chemistry letters · 2022Article
- Wnt/β-Catenin Signalling and Its Cofactor BCL9L Have an Oncogenic Effect in Bladder Cancer Cells.International journal of molecular sciences · 2022Article
- The interactions of Bcl9/Bcl9L with β-catenin and Pygopus promote breast cancer growth, invasion, and metastasis.Oncogene · 2021Article
- Discovery of an Orally Bioavailable Small-Molecule Inhibitor for the β-Catenin/B-Cell Lymphoma 9 Protein-Protein Interaction.Journal of medicinal chemistry · 2021Article
- Young Breast Cancer: Novel Gene Methylation in WBC.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- miR-140-3p inhibits colorectal cancer progression and its liver metastasis by targeting BCL9 and BCL2.Cancer medicine · 2021Article
- BCL9/BCL9L promotes tumorigenicity through immune-dependent and independent mechanisms in triple negative breast cancer.Oncogene · 2021Article
- Aberrations of Chromosomes 1 and 16 in Breast Cancer: A Framework for Cooperation of Transcriptionally Dysregulated Genes.Cancers · 2021Article
- Inhibition of the Wnt Signalling Pathway: An Avenue to Control Breast Cancer Aggressiveness.International journal of molecular sciences · 2020Review
- Wnt signaling in breast cancer: biological mechanisms, challenges and opportunities.Molecular cancer · 2020Review
- Long noncoding RNA BHLHE40-AS1 promotes early breast cancer progression through modulating IL-6/STAT3 signaling.Journal of cellular biochemistry · 2020Article
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Authors and funding
26 authors at 8 institutions in 1 country.
Funding
Abstract
introductionThere are an estimated 60,000 new cases of ductal carcinoma in situ (DCIS) each year. A lack of understanding in DCIS pathobiology has led to overtreatment of more than half of patients. We profiled the temporal molecular changes during DCIS transition to invasive ductal carcinoma (IDC) using in vivo DCIS progression models. These studies identified B cell lymphoma-9 (BCL9) as a potential molecular driver of early invasion. BCL9 is a newly found co-activator of Wnt-stimulated β-catenin-mediated transcription. BCL9 has been shown to promote progression of multiple myeloma and colon carcinoma. However BCL9 role in breast cancer had not been previously recognized.
methodsMicroarray and RNA sequencing were utilized to characterize the sequential changes in mRNA expression during DCIS invasive transition. BCL9-shRNA knockdown was performed to assess the role of BCL9 in in vivo invasion, epithelial-mesenchymal transition (EMT) and canonical Wnt-signaling. Immunofluorescence of 28 patient samples was used to assess a correlation between the expression of BCL9 and biomarkers of high risk DCIS. The cancer genome atlas data were analyzed to assess the status of BCL9 gene alterations in breast cancers.
resultsAnalysis of BCL9, by RNA and protein showed BCL9 up-regulation to be associated with DCIS transition to IDC. Analysis of patient DCIS revealed a significant correlation between high nuclear BCL9 and pathologic characteristics associated with DCIS recurrence: Estrogen receptor (ER) and progesterone receptor (PR) negative, high nuclear grade, and high human epidermal growth factor receptor2 (HER2). In vivo silencing of BCL9 resulted in the inhibition of DCIS invasion and reversal of EMT. Analysis of the TCGA data showed BCL9 to be altered in 26 % of breast cancers. This is a significant alteration when compared to HER2 (ERBB2) gene (19 %) and estrogen receptor (ESR1) gene (8 %). A significantly higher proportion of basal like invasive breast cancers compared to luminal breast cancers showed BCL9 amplification.
conclusionBCL9 is a molecular driver of DCIS invasive progression and may predispose to the development of basal like invasive breast cancers. As such, BCL9 has the potential to serve as a biomarker of high risk DCIS and as a therapeutic target for prevention of IDC.
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