ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Extracellular Vesicle-Packaged Linc-ZNF25-1 from Pancreatic Cancer Cell Promotes Pancreatic Stellate Cell Uptake of Asparagine to Advance Chemoresistance.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- ETV4 Promotes Colorectal Cancer Progression by Reprogramming Asparagine Metabolism to Remodel the Stromal Microenvironment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Metabolic Messengers: Extracellular Vesicles as Central Mediators of Metabolic Reprogramming in Renal Cell Cancer.Biomedicines · 2026Review
- F41, a Novel Fungal Indole-Diterpenoid, Overcomes Gemcitabine Resistance in Pancreatic Cancer by Inducing ER Stress.International journal of molecular sciences · 2025Article
- Extracellular Vesicle-Packaged Linc-ZNF25-1 from Pancreatic Cancer Cell Promotes Pancreatic Stellate Cell Uptake of Asparagine to Advance Chemoresistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Extensive fibrous stroma plays an important role in gemcitabine (GEM) resistance. However, the mechanism by which pancreatic cancer cells interact with pancreatic stellate cells (PSCs) to promote GEM resistance remains unclear. This study investigates the role of metabolic crosstalk between these two cells in inducing GEM resistance. Extracellular vesicles (EVs) of parental and GEM-resistant pancreatic cancer cells are extracted and performed metabolic assays and long noncoding RNA (lncRNA) sequencing. Pancreatic cancer cell-derived EVs promote PSCs activation and extracellular matrix formation, and GEM-resistant pancreatic cancer cells produce more asparagine (Asn), favoring PSCs activation. Mechanistically, pancreatic cancer cell-derived EVs mediate linc-ZNF25-1 to promote Asn uptake via the IGF2BP3/c-Myc/SLC1A5 pathway in PSCs. In addition, mouse models elucidate the oncogenic function of linc-ZNF25-1 and the enhanced therapeutic effect of asparaginase (L-ASNase) in combination with GEM in pancreatic cancer. This study demonstrates that pancreatic cancer cell-derived EVs promote the uptake of Asn released from pancreatic cancer cells through the upregulation of SLC1A5 in PSCs, facilitating PSCs activation and pancreatic cancer resistance to GEM. L-ASNase in combination with GEM is a potential therapeutic strategy for targeting stromal cells to enhance the efficacy of chemotherapeutic agents against pancreatic cancer.
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Registered trials
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