ReviewJournal of clinical medicine2013
The Roles of Epithelial-to-Mesenchymal Transition (EMT) and Mesenchymal-to-Epithelial Transition (MET) in Breast Cancer Bone Metastasis: Potential Targets for Prevention and Treatment.
Review in Journal of clinical medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
63 citing papers in PubMed, 99 citations in OpenAlex.
- TFF1-mediated suppression of the TCA cycle promotes bone metastasis in triple-negative breast cancer.Translational oncology · 2026Article
- Hijacking the bone niche: mechanistic insights into bone metastasis in breast cancer.Bone research · 2026Review
- Macrophage-derived extracellular vesicles in the remodeling of the prostate cancer immune microenvironment and therapeutic resistance.Journal of translational medicine · 2026Review
- SPP1 (osteopontin): a key regulator orchestrating cancer progression and non-cancerous pathologies - therapeutic opportunities and future directions.Frontiers in cell and developmental biology · 2026Review
- Exploring Molecular Mechanism of Thymoquinone via cMet and PDGFR for Accelerated Hemostasis: An Approach Through In Silico, In Vitro, and In Vivo Studies.Chemistry & biodiversity · 2026Article
- Article
- Boosting data interpretation with GIBOOST to enhance visualization of complex high-dimensional data.Briefings in bioinformatics · 2025Article
- Hypoxia-driven angiogenesis in breast cancer mechanisms and therapeutic targets: a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Oxygen deprivation in breast cancer: mechanisms, pathways, and implications.Annals of medicine and surgery (2012) · 2025Review
- DEC1 promotes breast cancer bone metastasis through transcriptional activation of CXCR4.Journal of biomedical research · 2025Article
- The Clinical Relevance of Epithelial-to-Mesenchymal Transition Hallmarks: A Cut-Off-Based Approach in Healthy and Cancerous Cell Lines.International journal of molecular sciences · 2025Article
- SQSTM1/p62 Mediates the Effects of CPNE3 on the Epithelialmesenchymal Transition and Migration Inhibition of Lung Adenocarcinoma Cells.Current medicinal chemistry · 2025Article
- Insight into prostate cancer osteolytic metastasis by RelB coordination of IL-8 and S100A4.Clinical and translational medicine · 2024Article
- Discovery of a novel hybrid coumarin-hydroxamate conjugate targeting the HDAC1-Sp1-FOSL2 signaling axis for breast cancer therapy.Cell communication and signaling : CCS · 2024Article
- Adipocyte-derived extracellular vesicles: bridging the communications between obesity and tumor microenvironment.Discover oncology · 2023Review
- Aberrant expression of bone morphogenetic proteins in the disease progression and metastasis of breast cancer.Frontiers in oncology · 2023Article
- RUNX2 recruits the NuRD(MTA1)/CRL4B complex to promote breast cancer progression and bone metastasis.Cell death and differentiation · 2022Article
- An Insight into Molecular Targets of Breast Cancer Brain Metastasis.International journal of molecular sciences · 2022Review
- The KDM6A-SPARCL1 axis blocks metastasis and regulates the tumour microenvironment of gastrointestinal stromal tumours by inhibiting the nuclear translocation of p65.British journal of cancer · 2022Article
- UDP-glucose dehydrogenase expression is upregulated following EMT and differentially affects intracellular glycerophosphocholine and acetylaspartate levels in breast mesenchymal cell lines.Molecular oncology · 2022Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many studies have revealed molecular connections between breast and bone. Genes, important in the control of bone remodeling, such as receptor activator of nuclear kappa (RANK), receptor activator of nuclear kappa ligand (RANKL), vitamin D, bone sialoprotein (BSP), osteopontin (OPN), and calcitonin, are expressed in breast cancer and lactating breast. Epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) effectors play critical roles during embryonic development, postnatal growth, and epithelial homeostasis, but also are involved in a number of pathological conditions, including wound repair, fibrosis, inflammation, as well as cancer progression and bone metastasis. Transforming growth factor β (TGFβ), insulin-like growth factor I & II (IGF I & II), platelet-derived growth factor (PDGF), parathyroid hormone-related protein (PTH(rP)), vascular endothelial growth factor (VEGF), epithelial growth factors II/I (ErbB/EGF), interleukin 6 (IL-6), IL-8, IL-11, IL-1, integrin αvβ3, matrix metalloproteinases (MMPs), catepsin K, hypoxia, notch, Wnt, bone morphogenetic proteins (BMP), and hedgehog signaling pathways are important EMT and MET effectors identified in the bone microenviroment facilitating bone metastasis formation. Recently, Runx2, an essential transcription factor in the regulation of mesenchymal cell differentiation into the osteoblast lineage and proper bone development, is also well-recognized for its expression in breast cancer cells promoting osteolytic bone metastasis. Understanding the precise mechanisms of EMT and MET in the pathogenesis of breast cancer bone metastasis can inform the direction of therapeutic intervention and possibly prevention.
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Registered trials
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.