ArticleScientific reports2023
Switching mechanism from AR to EGFR signaling via 3-O-sulfated heparan sulfate in castration-resistant prostate cancer.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Chondroitin sulfate E activates IL-6/STAT3 signaling to drive androgen-independent growth in castration-resistant prostate cancer.Cell communication and signaling : CCS · 2026Article
- The Glycosaminoglycan-Dependent Interactome of Neurexin-1 in Human Fetal Glial Cells.Proteoglycan research · 2025Article
- 3-O Sulfated Heparan Sulfate (G2) Peptide Ligand Impairs the Infectivity ofBiomolecules · 2025Article
- Development and experimental verification of a prognosis model for hypoxia- and lactate metabolism-associated genes in HNSCC.Medicine · 2025Article
- Androgen receptor-regulated lncRNA PRCAT71 promotes AR signaling through the interaction with KHSRP in prostate cancer.Science advances · 2025Article
- Synergistic anticancer effect of CDRI-08 and abiraterone acetate against castration resistant prostate cancer targeting PI3K/Akt pathway.Iranian journal of basic medical sciences · 2025Article
- The role of heparan sulfate in enhancing the chemotherapeutic response in triple-negative breast cancer.Breast cancer research : BCR · 2024Article
- Construction of mouse cochlin mutants with different GAG-binding specificities and their use for immunohistochemistry.The Biochemical journal · 2023Article
- SCAMP3 and EPS8 Cooperatively Regulate EGFR Signaling to Promote Enzalutamide Resistance and Metastatic Potential in Prostate Cancer.Cancer genomics & proteomicsArticle
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Androgen deprivation therapy is given to suppress prostate cancer growth; however, some cells continue to grow hormone-independently as castration-resistant prostate cancer (CRPC). Sulfated glycosaminoglycans promote ligand binding to receptors as co-receptors, but their role in CRPC remains unknown. Using the human prostate cancer cell line C4-2, which can proliferate in hormone-dependent and hormone-independent conditions, we found that epidermal growth factor (EGF)-activated EGFR-ERK1/2 signaling via 3-O-sulfated heparan sulfate (HS) produced by HS 3-O-sulfotransferase 1 (HS3ST1) is activated in C4-2 cells under hormone depletion. Knockdown of HS3ST1 in C4-2 cells suppressed hormone-independent growth, and inhibited both EGF binding to the cell surface and activation of EGFR-ERK1/2 signaling. Gefitinib, an EGFR inhibitor, significantly suppressed C4-2 cell proliferation and growth of a xenografted C4-2 tumor in castrated mouse. Collectively, our study has revealed a mechanism by which cancer cells switch to hormone-independent growth and identified the key regulator as 3-O-sulfated HS.
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