ArticleInternational journal of molecular sciences2014
Activation of VCAM-1 and its associated molecule CD44 leads to increased malignant potential of breast cancer cells.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 53 citations in OpenAlex.
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- Capillary constrictions prime cancer cell tumorigenicity through PIEZO1.Nature communications · 2025Article
- Mechanical Loading of Osteocytes via Oscillatory Fluid Flow Regulates Early-Stage PC-3 Prostate Cancer Metastasis to Bone.Advanced biology · 2025Article
- VCAM-1 as a common biomarker in inflammatory bowel disease and colorectal cancer: unveiling the dual anti-inflammatory and anti-cancer capacities of anti-VCAM-1 therapies.Cancer metastasis reviews · 2025Review
- Prioritization of drug targets for thyroid cancer: a multi-omics Mendelian randomization study.Endocrine · 2024Article
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- Cancer-associated fibroblasts: The chief architect in the tumor microenvironment.Frontiers in cell and developmental biology · 2023Review
- Recent progress in cancer cell membrane-based nanoparticles for biomedical applications.Beilstein journal of nanotechnology · 2023Review
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- The molecular mechanisms and therapeutic strategies of EMT in tumor progression and metastasis.Journal of hematology & oncology · 2022Review
- Analysis of gene expression profile of peripheral blood in alveolar and cystic echinococcosis.Frontiers in cellular and infection microbiology · 2022Article
- The tumor microenvironment as driver of stemness and therapeutic resistance in breast cancer: New challenges and therapeutic opportunities.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- High VCAM-1 Predicts Poor Prognosis and is Associated with Chemotherapy Resistance in Nasopharyngeal Carcinoma.OncoTargets and therapy · 2021Article
- Cancer Cell CD44 Mediates Macrophage/Monocyte-Driven Regulation of Head and Neck Cancer Stem Cells.Cancer research · 2020Article
- EMT-Associated Heterogeneity in Circulating Tumor Cells: Sticky Friends on the Road to Metastasis.Cancers · 2020Review
- VCAM-1 Upregulation Contributes to Insensitivity of Vemurafenib in BRAF-Mutant Thyroid Cancer.Translational oncology · 2020Article
- ST6GAL2 Downregulation Inhibits Cell Adhesion and Invasion and is Associated with Improved Patient Survival in Breast Cancer.OncoTargets and therapy · 2020Article
- Cisplatin-resistant triple-negative breast cancer subtypes: multiple mechanisms of resistance.BMC cancer · 2019Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
VCAM-1 (CD106), a transmembrane glycoprotein, was first reported to play an important role in leukocyte adhesion, leukocyte transendothelial migration and cell activation by binding to integrin VLA-1 (α4β1). In the present study, we observed that VCAM-1 expression can be induced in many breast cancer epithelial cells by cytokine stimulation in vitro and its up-regulation directly correlated with advanced clinical breast cancer stage. We found that VCAM-1 over-expression in the NMuMG breast epithelial cells controls the epithelial and mesenchymal transition (EMT) program to increase cell motility rates and promote chemoresistance to doxorubicin and cisplatin in vitro. Conversely, in the established MDAMB231 metastatic breast cancer cell line, we confirmed that knockdown of endogenous VCAM-1 expression reduced cell proliferation and inhibited TGFβ1 or IL-6 mediated cell migration, and increased chemosensitivity. Furthermore, we demonstrated that knockdown of endogenous VCAM-1 expression in MDAMB231 cells reduced tumor formation in a SCID xenograft mouse model. Signaling studies showed that VCAM-1 physically associates with CD44 and enhances CD44 and ABCG2 expression. Our findings uncover the possible mechanism of VCAM-1 activation facilitating breast cancer progression, and suggest that targeting VCAM-1 is an attractive strategy for therapeutic intervention.
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