ArticleCancer research2014
Runx2 is a novel regulator of mammary epithelial cell fate in development and breast cancer.
Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 74 citations in OpenAlex.
- Loss of MEG3 promotes migration and invasion of nickel-transformed cells, partially via upregulation of RUNX2.Toxicology and applied pharmacology · 2026Article
- Runx1 and Runx2 act in concert to suppress Wnt/β-catenin-driven mammary tumourigenesis.British journal of cancer · 2026Article
- PBRM1-dependent PBAF targeting is required for EMT and metastasis in breast cancer.Science advances · 2026Article
- RUNX2 cooperates with SREBP1 to rewire cancer metabolism and promote aggressiveness.Journal of experimental & clinical cancer research : CR · 2025Article
- Runx2 downregulates Lpl expression through super-silencer formation to alter lipid metabolism in Zhu Schwann cells after nerve injury.Cellular & molecular biology letters · 2025Article
- Overexpression of RUNX2 promotes breast cancer multi-organ metastasis through stabilizing c-Myc.Cell death & disease · 2025Article
- RUNX2 mediated epithelial mesenchymal transition induced by TGF beta and Smad signaling promotes malignant progression in glioma.Scientific reports · 2025Article
- Mechanisms of Regulation of Cell Fate in Breast Development and Cancer.Advances in experimental medicine and biology · 2025Review
- Exploring the transcriptional cooperation between RUNX2 and its associated elncRNA RAIN.Cell death & disease · 2024Article
- Article
- Cecal microbiota and mammary gland microRNA signatures are related and modifiable by dietary flaxseed with implications for breast cancer risk.Microbiology spectrum · 2024Article
- FGFR2 genetic variants in women with breast cancer.Molecular medicine reports · 2023Article
- Cell type and stage specific transcriptional, chromatin and cell-cell communication landscapes in the mammary gland.Heliyon · 2023Article
- Review
- Role of RUNX2 in breast cancer development and drug resistance (Review).Oncology letters · 2023Review
- Review
- Article
- RUNX3 in Stem Cell and Cancer Biology.Cells · 2023Review
- RUNX2 promotes gastric cancer progression through the transcriptional activation of MGAT5 and MMP13.Frontiers in oncology · 2023Article
- Dissecting the molecular trajectory of fibroblast reprogramming to chemically induced mammary epithelial cells.Frontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Regulators of differentiated cell fate can offer targets for managing cancer development and progression. Here, we identify Runx2 as a new regulator of epithelial cell fate in mammary gland development and breast cancer. Runx2 is expressed in the epithelium of pregnant mice in a strict temporally and hormonally regulated manner. During pregnancy, Runx2 genetic deletion impaired alveolar differentiation in a manner that disrupted alveolar progenitor cell populations. Conversely, exogenous transgenic expression of Runx2 in mammary epithelial cells blocked milk production, suggesting that the decrease in endogenous Runx2 observed late in pregnancy is necessary for full differentiation. In addition, overexpression of Runx2 drove epithelial-to-mesenchymal transition-like changes in normal mammary epithelial cells, whereas Runx2 deletion in basal breast cancer cells inhibited cellular phenotypes associated with tumorigenesis. Notably, loss of Runx2 expression increased tumor latency and enhanced overall survival in a mouse model of breast cancer, with Runx2-deficient tumors exhibiting reduced cell proliferation. Together, our results establish a previously unreported function for Runx2 in breast cancer that may offer a novel generalized route for therapeutic interventions. Cancer Res; 74(18); 5277-86. ©2014 AACR.
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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.