ArticlePloS one2014
Chondroitin sulfate-E is a negative regulator of a pro-tumorigenic Wnt/beta-catenin-Collagen 1 axis in breast cancer cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 62 citations in OpenAlex.
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- Integrating plasma protein-centric multi-omics to identify potential therapeutic targets for pancreatic cancer.Journal of translational medicine · 2024Article
- CSGALNACT2 restricts ovarian cancer migration and invasion by modulating MAPK/ERK pathway through DUSP1.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Sulfation of chondroitin and bile acids converges to antagonize Wnt/Acta pharmaceutica Sinica. B · 2024Article
- In silico analysis of differentially expressed-aberrantly methylated genes in breast cancer for prognostic and therapeutic targets.Clinical and experimental medicine · 2023Article
- The Southern European Atlantic Diet and Its Supplements: The Chemical Bases of Its Anticancer Properties.Nutrients · 2023Review
- Mutant MESD links cellular stress to type I collagen aggregation in osteogenesis imperfecta type XX.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- Review
- Suppression of the malignancy of mammary tumor in mice model by inactivated preparation ofVeterinary research forum : an international quarterly journal · 2022Article
- Modeling extracellular matrix through histo-molecular gradient in NSCLC for clinical decisions.Frontiers in oncology · 2022Article
- Chondroitin Sulfates Control Invasiveness of the Basal-Like Breast Cancer Cell Line MDA-MB-231 Through ROR1.Frontiers in oncology · 2022Article
- Infrared Microspectroscopy and Imaging Analysis of Inflammatory and Non-Inflammatory Breast Cancer Cells and Their GAG Secretome.Molecules (Basel, Switzerland) · 2020Article
- Enzymatic Synthesis of Chondroitin Sulfate E to Attenuate Bacteria Lipopolysaccharide-Induced Organ Damage.ACS central science · 2020Article
- Distinct diagnostic and prognostic values of γ-aminobutyric acid type A receptor family genes in patients with colon adenocarcinoma.Oncology letters · 2020Article
- Proteoglycan serglycin promotes non-small cell lung cancer cell migration through the interaction of its glycosaminoglycans with CD44.Journal of biomedical science · 2020Article
- Galactosaminoglycans: Medical Applications and Drawbacks.Molecules (Basel, Switzerland) · 2019Review
- The dual role of the glycosaminoglycan chondroitin-6-sulfate in the development, progression and metastasis of cancer.The FEBS journal · 2019Review
- Identification of hub genes and therapeutic drugs in esophageal squamous cell carcinoma based on integrated bioinformatics strategy.Cancer cell international · 2019Article
- Galectin-3 Regulates the Expression of Tumor Glycosaminoglycans and Increases the Metastatic Potential of Breast Cancer.Journal of oncology · 2019Article
- COL1A1 promotes metastasis in colorectal cancer by regulating the WNT/PCP pathway.Molecular medicine reports · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of the glycosaminoglycan chondroitin sulfate-E (CS-E) is misregulated in many human cancers, including breast cancer. Cell-surface associated CS-E has been shown to have pro-tumorigenic functions, and pharmacological treatment with exogenous CS-E has been proposed to interfere with tumor progression mediated by endogenous CS-E. However, the effects of exogenous CS-E on breast cancer cell behavior, and the molecular mechanisms deployed by CS-E are not well understood. We show here that treatment with CS-E, but not other chondroitin forms, could interfere with the invasive protrusion formation and migration of breast cancer cells in three-dimensional organotypic cultures. Microarray analysis identified transcriptional programs controlled by CS-E in these cells. Importantly, negative regulation of the pro-metastatic extracellular matrix gene Col1a1 was required for the anti-migratory effects of exogenous CS-E. Knock-down of Col1a1 gene expression mimics the effects of CS-E treatment, while exposing cells to a preformed collagen I matrix interfered with the anti-migratory effects of CS-E. In addition, CS-E specifically interfered with Wnt/beta-catenin signaling, a known pro-tumorigenic pathway. Lastly, we demonstrate that Col1a1 is a positively regulated target gene of the Wnt/beta-catenin pathway in breast cancer cells. Together, our data identify treatment with exogenous CS-E as negative regulatory mechanism of breast cancer cell motility through interference with a pro-tumorigenic Wnt/beta-catenin-Collagen I axis.
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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.