ArticleBMC cancer2015
SDF-1alpha concentration dependent modulation of RhoA and Rac1 modifies breast cancer and stromal cells interaction.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 21 citations in OpenAlex.
- Xiaotan Sanjie recipe suppressed the oncogenic potential of cancer-associated fibroblaststhe stromal-derived factor 1α/C-X-C chemokine receptor type 4 pathway in gastric cancer.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Mineralized Cryogel/Hydrogel Constructs to Recapitulate Early Breast Cancer Bone Metastasis In Vitro.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- CXCL12 and CXCR4 as Potential Early Biomarkers for Luminal A and Luminal B Subtypes of Breast Cancer.Cancer management and research · 2023Article
- Akt-Activated Endothelium Increases Cancer Cell Proliferation and Resistance to Treatment in Ovarian Cancer Cell Organoids.International journal of molecular sciences · 2022Article
- Review
- Rac1, A Potential Target for Tumor Therapy.Frontiers in oncology · 2021Review
- Review
- Angiocrine endothelium: from physiology to cancer.Journal of translational medicine · 2020Review
- Akt-activated endothelium promotes ovarian cancer proliferation through notch activation.Journal of translational medicine · 2019Article
- Surgical peritoneal stress creates a pro-metastatic niche promoting resistance to apoptosis via IL-8.Journal of translational medicine · 2018Article
- CCL2/CCL5 secreted by the stroma induce IL-6/PYK2 dependent chemoresistance in ovarian cancer.Molecular cancer · 2018Article
- Halfway between 2D and Animal Models: Are 3D Cultures the Ideal Tool to Study Cancer-Microenvironment Interactions?International journal of molecular sciences · 2018Review
- CXCL12 induces migration of Schwann cells via p38 MAPK and autocrine of CXCL12 by the CXCR4 receptor.International journal of clinical and experimental pathology · 2018Article
- Roles of Ras Homolog A in Invasive Ductal Breast Carcinoma.Acta histochemica et cytochemica · 2016Article
- VE-cadherin cleavage by ovarian cancer microparticles induces β-catenin phosphorylation in endothelial cells.Oncotarget · 2016Article
- Chemokine receptor CXCR4 activates the RhoA/ROCK2 pathway in spinal neurons that induces bone cancer pain.Molecular painArticle
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe interaction of SDF-1alpha with its receptor CXCR4 plays a role in the occurrence of distant metastasis in many solid tumors. This interaction increases migration from primary sites as well as homing at distant sites.
methodsHere we investigated how SDF-1α could modulate both migration and adhesion of cancer cells through the modulation of RhoGTPases.
resultsWe show that different concentrations of SDF-1α modulate the balance of adhesion and migration in cancer cells. Increased migration was obtained at 50 and 100 ng/ml of SDF-1α; however migration was reduced at 200 ng/ml. The adhesion between breast cancer cells and BMHC was significantly increased by SDF-1α treatment at 200 ng/ml and reduced using a blocking monoclonal antibody against CXCR4. We showed that at low SDF-1α concentration, RhoA was activated and overexpressed, while at high concentration Rac1 was promoting SDF-1α mediating-cell adhesion.
conclusionWe conclude that SDF-1α concentration modulates migration and adhesion of breast cancer cells, by controlling expression and activation of RhoGTPases.
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