ArticleActa pharmacologica Sinica2010
Transforming growth factor-beta1 upregulates the expression of CXC chemokine receptor 4 (CXCR4) in human breast cancer MCF-7 cells.
Article in Acta pharmacologica Sinica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 57 citations in OpenAlex.
- A single-domain i-body, AD-114, attenuates renal fibrosis through blockade of CXCR4.JCI insight · 2022Article
- A Novel Necroptosis-Associated lncRNA Signature Can Impact the Immune Status and Predict the Outcome of Breast Cancer.Journal of immunology research · 2022Article
- Role and clinical significance of TGF‑β1 and TGF‑βR1 in malignant tumors (Review).International journal of molecular medicine · 2021Review
- Gefitinib promotes CXCR4-dependent epithelial to mesenchymal transition via TGF-β1 signaling pathway in lung cancer cells harboring EGFR mutation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- CXCR7 promotes migration and invasion in head and neck squamous cell carcinoma by upregulating TGF-β1/Smad2/3 signaling.Scientific reports · 2019Article
- The role of CXCR4 in multiple myeloma: Cells' journey from bone marrow to beyond.Journal of bone oncology · 2019Review
- Local CXCR4 Upregulation in the Injured Arterial Wall Contributes to Intimal Hyperplasia.Stem cells (Dayton, Ohio) · 2016Article
- Article
- Intrinsic TGF-β2-triggered SDF-1-CXCR4 signaling axis is crucial for drug resistance and a slow-cycling state in bone marrow-disseminated tumor cells.Oncotarget · 2015Article
- A Tale from TGF-β Superfamily for Thymus Ontogeny and Function.Frontiers in immunology · 2015Review
- Immunohistochemical expression of CXCR4 on breast cancer and its clinical significance.Analytical cellular pathology (Amsterdam) · 2015Review
- CXCL12 chemokine and GABA neurotransmitter systems crosstalk and their putative roles.Frontiers in cellular neuroscience · 2014Review
- Baclofen and other GABAB receptor agents are allosteric modulators of the CXCL12 chemokine receptor CXCR4.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- The Role of chemokine receptor CXCR4 in breast cancer metastasis.American journal of cancer research · 2013Article
- TGF-β polymorphism and its expression correlated with CXCR4 expression in human breast cancer.Molecular biology reports · 2012Article
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10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate whether rhTGF-beta1 or a recombinant vector encoding a fusion protein comprising an extracellular domain of TGF-beta receptor II and an IgG Fc fragment) affects the regulation of CXC chemokine receptor 4 (CXCR4) expression in MCF-7 human breast cancer cells.
methodsMCF-7 breast cancer cells were treated with rhTGF-beta1 or transfected with a recombinant vector, pIRES2-EGFP-TbetaRII-Fc. Expression of CXCR4 in these cells was then analyzed at the mRNA and protein levels by quantitative RT-PCR and flow cytometry assay, respectively. A transwell assay was used to measure the chemotactic response of these cells to SDF-1alpha.
resultsCXCR4 mRNA and protein expression were upregulated in TGF-beta1-treated MCF-7 cells. These cells also demonstrated an enhanced chemotactic response to SDF-1alpha. In MCF-7 cells transiently transfected with pIRES2-EGFP-TbetaRII-Fc, a fusion protein named TbetaRII-Fc (approximately 41 kDa) was produced and secreted. In these transfected cells, there was a reduction in CXCR4 expression and in the SDF-1alpha-mediated chemotactic response.
conclusionTGF-beta1 upregulated CXCR4 expression in MCF-7 cells, which subsequently enhanced the SDF-1alpha-induced chemotactic response. The results suggest a link between TGF-beta1 and CXCR4 expression in MCF-7 human breast cancer cells, which may be one of the mechanisms of TGF-beta1-mediated enhancement of metastatic potential in breast cancer cells.
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