ArticleBritish journal of cancer2026
Cancer-associated fibroblast-derived GAS6 increases resistance to chemotherapy through AXL/STAT3/ABCG1 in gastric cancer.
Article in British journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The trial behind it
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Who cites it
5 citing papers in PubMed.
- AXL at the nexus of therapeutic resistance, tumor vascularization, and immune evasion in cancer.iScience · 2026Review
- AXL is associated with STAT3 activation in breast cancer.Molecular and clinical oncology · 2026Article
- Sphingosine-1-phosphate induces angiogenesis via the activating STAT3 signaling pathway to drive colorectal cancer progression.Journal of gastrointestinal oncology · 2026Article
- C3Journal of translational medicine · 2026Article
- Therapy-educated fibroblast states link treatment pressure to residual disease and acquired resistance in gastric cancer.Frontiers in immunology · 2026Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChemoresistance induced by cancer-associated fibroblasts (CAFs) is well recognized, yet its mechanisms remain unclear and no CAF-targeted therapies are available. Gastric cancer (GC) with extensive CAF infiltration correlates with poor prognosis, and emerging evidence highlights the GAS6/AXL axis in CAF-GC interactions. This study targets GAS6/AXL axis to overcome CAF-mediated chemoresistance and enhance chemotherapy efficacy.
methodsWe investigated the effect of 9im, a selective AXL inhibitor, on CAF-induced chemoresistance in GC using transwell migration, western blotting, viability assays, flow cytometry, drug efflux assays and in vivo experiments. Transcriptome analysis identified chemoresistance-related genes, and luciferase assays assessed STAT3 binding to the ABCG1 promoter. RNA-ISH analyzed GAS6
resultsGAS6 expression was elevated in CAF. CAF-derived GAS6 promoted GC cell migration and chemoresistance via AXL activation, effects reversed by 9im. STAT3 bound to the ABCG1 promoter, enhancing expression, while STAT3 inhibition reduced ABCG1 levels. 9im restored chemosensitivity in GC models. Clinically, ABCG1 and CAF marker co-expression correlated with poor prognosis.
conclusionsCAF-derived GAS6 induces GC chemoresistance via the AXL/STAT3/ABCG1 pathway. 9im restores chemosensitivity by inhibiting AXL and ABCG1-mediated efflux. AXL inhibitors with chemotherapy may improve GC treatment.
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