Hypoxia and TGF-β Drive Breast Cancer Bone Metastases through Parallel Signaling Pathways in Tumor Cells and the Bone Microenvironment
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Summary
Hypoxia and TGF-β signaling in parallel drive tumor bone metastases and regulate a common set of tumor genes, and small molecule inhibitors, by acting on both tumor cells and the bone microenvironment, additively decrease tumor burden, while improving skeletal quality.
- Type
- article
- Published
- 2009-09-03
- Cited by
- 219
- References
- 114
- Access
- Open access
- OpenAlex
- https://openalex.org/W2002267320
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:13066323
Keywords
Hypoxia (environmental), Tumor microenvironment, Cancer research, Signal transduction, Breast cancer
References
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Cited by
- Bone Metastasis of Breast Cancer.
- Hypoxia and metastasis in breast cancer.
- Altered gene products involved in the malignant reprogramming of cancer stem/progenitor cells and multitargeted therapies
- Epithelial-to-mesenchymal transition: what is the impact on breast cancer stem cells and drug resistance.
- The TGFβ Signaling Regulator PMEPA1 Suppresses Prostate Cancer Metastases to Bone
- Cancer-associated muscle weakness: What's bone got to do with it?
- Breast Cancer Metastasis: Are Cytokines Important Players During Its Development and Progression?
- Application of a human bone engineering platform to an in vitro and in vivo breast cancer metastasis model
- Novel Mechanisms and Therapeutics in the Treatment for Cancer-Induced Bone Pain
- Non-Invasive Quantitative Imaging Informs Early Assessment of Cancer Therapeutic Response.
- The Hypoxic Tumor Microenvironment: A Driving Force for Breast Cancer Progression
- The role of the chemokine receptor CXCR4 in EGFRvIII-expressing breast cancer
- Régulation de l’activité transcriptionnelle des récepteurs des estrogènes (ER) par le récepteur à chimiokine CXCR4 et les récepteurs à activité tyrosine kinase ErbB2 et ErbB3
- Bone marrow as a metastatic niche for disseminated tumor cells from solid tumors.
- New therapeutic targets for cancer bone metastases
- TGFβ modulated changes in VEGF expression and secretion may enhance disease progression through an autocrine mechanism
- Hypoxia-inducible factor 1 mediates TAZ expression and nuclear localization to induce the breast cancer stem cell phenotype
- ATF4 promotes bone angiogenesis by increasing VEGF expression and release in the bone environment
- The activity of the TGF beta superfamily in prostate cancer and the formation of bone metastases.
- The Role of chemokine receptor CXCR4 in breast cancer metastasis.
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