ArticleMolecular cancer2010
The Runx transcriptional co-activator, CBFbeta, is essential for invasion of breast cancer cells.
Article in Molecular cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 63 citations in OpenAlex.
- Review
- Transcription factor E2F8 is a therapeutic target in the basal-like subtype of breast cancer.Frontiers in oncology · 2023Article
- Review
- Transcription factor Runx2 changes the expression of some matricellular proteins in metastatic breast cancer cells.Molecular biology reports · 2022Article
- Cancer-Associated Exosomal CBFB Facilitates the Aggressive Phenotype, Evasion of Oxidative Stress, and Preferential Predisposition to Bone Prometastatic Factor of Breast Cancer Progression.Disease markers · 2022Article
- CBFβ promotes colorectal cancer progression through transcriptionally activating OPN, FAM129A, and UPP1 in a RUNX2-dependent manner.Cell death and differentiation · 2021Article
- The mutational landscape of the SCAN-B real-world primary breast cancer transcriptome.EMBO molecular medicine · 2020Article
- RUNX2/CBFB modulates the response to MEK inhibitors through activation of receptor tyrosine kinases in KRAS-mutant colorectal cancer.Translational oncology · 2020Article
- Identification of the hub genes RUNX2 and FN1 in gastric cancer.Open medicine (Warsaw, Poland) · 2020Article
- Targeting transcription factors in cancer - from undruggable to reality.Nature reviews. Cancer · 2019Review
- Transcriptional activation of CBFβ by CDK11Cell communication and signaling : CCS · 2019Article
- The cancer-related transcription factor RUNX2 modulates expression and secretion of the matricellular protein osteopontin in osteosarcoma cells to promote adhesion to endothelial pulmonary cells and lung metastasis.Journal of cellular physiology · 2019Article
- CBFβ/RUNX3-miR10b-TIAM1 molecular axis inhibits proliferation, migration, and invasion of gastric cancer cells.International journal of clinical and experimental pathology · 2019Article
- A role for the unfolded protein response stress sensor ERN1 in regulating the response to MEK inhibitors in KRAS mutant colon cancers.Genome medicine · 2018Article
- Antitumor efficacy of the Runx2-dendritic cell vaccine in triple-negative breast cancerOncology letters · 2018Article
- Impact of RUNX2 on drug-resistant human pancreatic cancer cells with p53 mutations.BMC cancer · 2018Review
- Characterization of CADD522, a small molecule that inhibits RUNX2-DNA binding and exhibits antitumor activity.Oncotarget · 2017Article
- Integrated RNA-seq and DNase-seq analyses identify phenotype-specific BMP4 signaling in breast cancer.BMC genomics · 2017Article
- Novel Implications of DNA Damage Response in Drug Resistance of Malignant Cancers Obtained from the Functional Interaction between p53 Family and RUNX2.Biomolecules · 2015Review
- RUNX2 and the PI3K/AKT axis reciprocal activation as a driving force for tumor progression.Molecular cancer · 2015Review
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4 authors at 1 institution in 1 country.
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Abstract
backgroundThe transcription factor Runx2 has an established role in cancers that metastasize to bone. In metastatic breast cancer cells Runx2 is overexpressed and contributes to the invasive capacity of the cells by regulating the expression of several invasion genes. CBFbeta is a transcriptional co-activator that is recruited to promoters by Runx transcription factors and there is considerable evidence that CBFbeta is essential for the function of Runx factors. However, overexpression of Runx1 can partially rescue the lethal phenotype in CBFbeta-deficient mice, indicating that increased levels of Runx factors can, in some situations, overcome the requirement for CBFbeta. Since Runx2 is overexpressed in metastatic breast cancer cells, and there are no reports of CBFbeta expression in breast cells, we sought to determine whether Runx2 function in these cells was dependent on CBFbeta. Such an interaction might represent a viable target for therapeutic intervention to inhibit bone metastasis.
resultsWe show that CBFbeta is expressed in the metastatic breast cancer cells, MDA-MB-231, and that it associates with Runx2. Matrigel invasion assays and RNA interference were used to demonstrate that CBFbeta contributes to the invasive capacity of these cells. Subsequent analysis of Runx2 target genes in MDA-MB-231 cells revealed that CBFbeta is essential for the expression of Osteopontin, Matrixmetalloproteinase-13, Matrixmetalloproteinase-9, and Osteocalcin but not for Galectin-3. Chromatin immunoprecipitation analysis showed that CBFbeta is recruited to both the Osteopontin and the Galectin-3 promoters.
conclusionsCBFbeta is expressed in metastatic breast cancer cells and is essential for cell invasion. CBFbeta is required for expression of several Runx2-target genes known to be involved in cell invasion. However, whilst CBFbeta is essential for invasion, not all Runx2-target genes require CBFbeta. We conclude that CBFbeta is required for a subset of Runx2-target genes that are sufficient to maintain the invasive phenotype of the cells. These findings suggest that the interaction between Runx2 and CBFbeta might represent a viable target for therapeutic intervention to inhibit bone metastasis.
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