ArticleCancer biology & medicine2026
VDAC1 protein derived from extracellular vesicles promotes paclitaxel resistance in gastric cancer through autophagy and mitophagy.
Article in Cancer biology & medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Advances in paclitaxel-mediated remodeling of the gastric cancer immune microenvironment and sensitization to immune checkpoint inhibitors via cGAS-STING pathway activation triggered by mtDNA release: challenges and translational perspectives.Molecular biology reports · 2026Review
- New Functions of Mitochondrial Dysfunction in Gastric Cancer: From Molecular Processes to Potential Treatments.International journal of molecular sciences · 2026Review
- ST6GAL1 promotes cancer stem-like cell-associated paclitaxel resistance through the EGFR-mTOR-SOX2/BMI1 axis in non-small cell lung cancer.Cancer drug resistance (Alhambra, Calif.) · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
objectivePaclitaxel (PTX), a conventional second-line therapeutic agent for advanced gastric cancer (GC), exhibits compromised clinical efficacy due to acquired chemoresistance in patients, the molecular mechanisms of which remain poorly elucidated. This study aimed to investigate the therapeutic potential of targeting extracellular vesicle (EV) protein in reversing PTX resistance in GC cells and to delineate the underlying molecular pathways involved.
methodsProteomic profiling was used to identify differentially expressed EV proteins in PTX-resistant GC cells. EVs were isolated
resultsProteomic analyses demonstrated a marked upregulation of VDAC1 in EVs secreted by PTX-resistant GC cells. Functional studies revealed that intercellular transfer of EV-derived VDAC1 directly conferred PTX resistance to drug-sensitive cancer cells. Gene set enrichment analysis (GSEA) and adenosine triphosphate (ATP) functional assay further elucidated that VDAC1-mediated chemoresistance was mechanistically linked to the activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) signaling and concomitant suppression of the mammalian target of rapamycin - p70 ribosomal protein S6 kinase (mTOR-p70S6K) pathway.
conclusionsThe findings herein underscore the pivotal role of EV-derived VDAC1 in driving PTX resistance in GC through dual modulation of autophagy and mitophagy, mediated by the AMPK/mTOR signaling axis. Targeting EV-derived VDAC1 has emerged as a promising therapeutic strategy to counteract chemoresistance, providing a novel avenue for improving GC treatment outcomes.
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