ArticleCancer science2020
HS2ST1-dependent signaling pathways determine breast cancer cell viability, matrix interactions, and invasive behavior.
Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
The trial behind it
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
16 citing papers in PubMed, 23 citations in OpenAlex.
- HS6ST1 regulates acute myeloid leukemia chemotherapy resistance via TGF-β1 signaling.Research square · 2026Article
- Regulatory Genomic Circuitry of Brain Age by Integrative Functional Genomic Analyses.Genomics, proteomics & bioinformatics · 2025Article
- Prognostic significance of HS2ST1 expression in patients with hepatocellular carcinoma.Genes & genomics · 2024Article
- MEG3-Mediated Oral Squamous-Cell-Carcinoma-Derived Exosomal miR-421 Activates Angiogenesis by Targeting HS2ST1 in Vascular Endothelial Cells.International journal of molecular sciences · 2024Article
- Advances in prognostic models for osteosarcoma risk.Heliyon · 2024Review
- Revisiting the Syndecans: Master Signaling Regulators with Prognostic and Targetable Therapeutic Values in Breast Carcinoma.Cancers · 2023Review
- Two novel predictive biomarkers for osteosarcoma and glycolysis pathways: A profiling study on HS2ST1 and SDC3.Medicine · 2022Article
- Identification of risk model based on glycolysis-related genes in the metastasis of osteosarcoma.Frontiers in endocrinology · 2022Article
- Differential Impact of Membrane-Bound and Soluble Forms of the Prognostic Marker Syndecan-1 on the Invasiveness, Migration, Apoptosis, and Proliferation of Cervical Cancer Cells.Frontiers in oncology · 2022Article
- HA and HS Changes in Endothelial Inflammatory Activation.Biomolecules · 2021Article
- Syndecan-4 as a Pathogenesis Factor and Therapeutic Target in Cancer.Biomolecules · 2021Review
- Heparan Sulfate Biosynthesis and Sulfation Profiles as Modulators of Cancer Signalling and Progression.Frontiers in oncology · 2021Review
- Infrared Microspectroscopy and Imaging Analysis of Inflammatory and Non-Inflammatory Breast Cancer Cells and Their GAG Secretome.Molecules (Basel, Switzerland) · 2020Article
- Heparan Sulfate Proteoglycan Signaling in Tumor Microenvironment.International journal of molecular sciences · 2020Review
- HS2ST1-dependent signaling pathways determine breast cancer cell viability, matrix interactions, and invasive behavior.Cancer science · 2020Article
- The Heparan Sulfate Sulfotransferases HS2ST1 and HS3ST2 Are Novel Regulators of Breast Cancer Stem-Cell Properties.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
15 authors at 8 institutions in 5 countries.
Funding
Abstract
Heparan sulfate proteoglycans (HSPGs) act as signaling co-receptors by interaction of their sulfated glycosaminoglycan chains with numerous signaling molecules. In breast cancer, the function of heparan sulfate 2-O-sulfotransferase (HS2ST1), the enzyme mediating 2-O-sulfation of HS, is largely unknown. Hence, a comparative study on the functional consequences of HS2ST1 overexpression and siRNA knockdown was performed in the breast cancer cell lines MCF-7 and MDA-MB-231. HS2ST1 overexpression inhibited Matrigel invasion, while its knockdown reversed the phenotype. Likewise, cell motility and adhesion to fibronectin and laminin were affected by altered HS2ST1 expression. Phosphokinase array screening revealed a general decrease in signaling via multiple pathways. Fluorescent ligand binding studies revealed altered binding of fibroblast growth factor 2 (FGF-2) to HS2ST1-expressing cells compared with control cells. HS2ST1-overexpressing cells showed reduced MAPK signaling responses to FGF-2, and altered expression of epidermal growth factor receptor (EGFR), E-cadherin, Wnt-7a, and Tcf4. The increased viability of HS2ST1-depleted cells was reduced to control levels by pharmacological MAPK pathway inhibition. Moreover, MAPK inhibitors generated a phenocopy of the HS2ST1-dependent delay in scratch wound repair. In conclusion, HS2ST1 modulation of breast cancer cell invasiveness is a compound effect of altered E-cadherin and EGFR expression, leading to altered signaling via MAPK and additional pathways.
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Registered trials
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.