ArticleNature communications2022
Reformation of the chondroitin sulfate glycocalyx enables progression of AR-independent prostate cancer.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Dual Compartmentalization of GSTA4 Suppresses Ferroptosis to Drive Antiandrogen Resistance in Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Chondroitin sulfate shapes the unfolded protein response in osteosarcoma to sustain cancer cell survival during ER stress.Cell death & disease · 2026Article
- Sweet and Bright: Illuminating Glycoprotein-Mediated Endocytosis via Metabolic Labeling and NanoLuciferase.ACS chemical biology · 2026Article
- Tumour acidosis remodels the glycocalyx to control lipid scavenging and ferroptosis.Nature cell biology · 2026Article
- Chondroitin sulfate E activates IL-6/STAT3 signaling to drive androgen-independent growth in castration-resistant prostate cancer.Cell communication and signaling : CCS · 2026Article
- Glycocalyx hyaluronan removal-induced increasing of cell stiffness delays breast cancer cells progression.Cellular and molecular life sciences : CMLS · 2025Article
- Transient CAR T cells with specificity to oncofetal glycosaminoglycans in solid tumors.EMBO molecular medicine · 2024Article
- Discriminating Benign from Malignant Lung Diseases Using Plasma Glycosaminoglycans and Cell-Free DNA.International journal of molecular sciences · 2024Article
- Tumor-agnostic cancer therapy using antibodies targeting oncofetal chondroitin sulfate.Nature communications · 2024Article
- Rapid cellular uptake of citrate-coated iron oxide nanoparticles unaffected by cell-surface glycosaminoglycans.Nanoscale advances · 2024Article
- Treatment-induced stemness and lineage plasticity in driving prostate cancer therapy resistance.Cancer heterogeneity and plasticity · 2024Article
- Proteoglycans: a common portal for SARS-CoV-2 and extracellular vesicle uptake.American journal of physiology. Cell physiology · 2023Review
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Authors and funding
26 authors at 6 institutions in 7 countries.
Funding
Abstract
Lineage plasticity of prostate cancer is associated with resistance to androgen receptor (AR) pathway inhibition (ARPI) and supported by a reactive tumor microenvironment. Here we show that changes in chondroitin sulfate (CS), a major glycosaminoglycan component of the tumor cell glycocalyx and extracellular matrix, is AR-regulated and promotes the adaptive progression of castration-resistant prostate cancer (CRPC) after ARPI. AR directly represses transcription of the 4-O-sulfotransferase gene CHST11 under basal androgen conditions, maintaining steady-state CS in prostate adenocarcinomas. When AR signaling is inhibited by ARPI or lost during progression to non-AR-driven CRPC as a consequence of lineage plasticity, CHST11 expression is unleashed, leading to elevated 4-O-sulfated chondroitin levels. Inhibition of the tumor cell CS glycocalyx delays CRPC progression, and impairs growth and motility of prostate cancer after ARPI. Thus, a reactive CS glycocalyx supports adaptive survival and treatment resistance after ARPI, representing a therapeutic opportunity in patients with advanced prostate cancer.
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