ArticleInternational journal of oncology2019
Paclitaxel‑resistant gastric cancer MGC‑803 cells promote epithelial‑to‑mesenchymal transition and chemoresistance in paclitaxel‑sensitive cells via exosomal delivery of miR‑155‑5p.
Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.
- Roles of microRNAs and exosomes in Helicobacter pylori associated gastric cancer.Molecular biology reports · 2023Pooled it
- Unraveling the Mechanisms of Chemoresistance in Gastric Cancer: Insights and Emerging Research Strategies.Current oncology reports · 2026Review
- Extracellular vesicles in gastric cancer: biological functions, clinical applications, and engineering strategies.Medical oncology (Northwood, London, England) · 2026Review
- Mechanisms of Paclitaxel Resistance: Recent Advances and Future Perspectives.International journal of molecular sciences · 2026Review
- Comprehensive Review of the Interplay of MicroRNA and Epithelial-Mesenchymal Transition in Radiation Resistance of Cancer.International journal of molecular sciences · 2026Review
- Tumor-Infiltrating Nociceptor Neurons in Ovarian Cancer Treatment Resistance.Advanced biology · 2026Article
- Tumor microenvironment dynamics in gastric cancer pathogenesis and therapeutic resistance.Molecular cancer · 2026Review
- Exosome-orchestrated network in gastric cancer: mechanisms, immune regulation, biomarkers and therapeutic vehicles.Frontiers in cell and developmental biology · 2026Review
- miR-155 aberrant expression impairs tumor rejection because of its targeting of ICOSL and multiple pathways implicated in the antitumor response.Pharmacological reviews · 2026Review
- From inflammation to carcinogenesis: MiRNA regulates epithelial-mesenchymal transition to facilitate malignant progression of gastric precancerous lesions.Frontiers in oncology · 2026Review
- Extracellular Vesicle-Derived microRNAs: Novel Non-Invasive Biomarkers for Gastrointestinal Malignancies.International journal of molecular sciences · 2025Review
- Article
- Increased expression of FBW7 may improve the prognosis of lung adenocarcinoma after pemetrexed chemotherapy by transforming the epithelial-to-mesenchymal process.Journal of thoracic disease · 2025Article
- Extracellular Vesicles as Mediators and Potential Targets in Combating Cancer Drug Resistance.Molecules (Basel, Switzerland) · 2025Review
- Functions and Clinical Applications of Exosomes in Gastric Cancer.International journal of biological sciences · 2025Review
- MicroRNA-155 and its exosomal form: Small pieces in the gastrointestinal cancers puzzle.Cell biology and toxicology · 2024Review
- The role of microRNAs in the gastric cancer tumor microenvironment.Molecular cancer · 2024Review
- Oxaliplatin-induced upregulation of exosomal miR-424-3p derived from human bone marrow mesenchymal stem cells attenuates progression of gastric cancer cells.Scientific reports · 2024Article
- Review
- Emerging Roles of Small Extracellular Vesicles in Gastrointestinal Cancer Research and Therapy.Cancers · 2024Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paclitaxel is a first‑line chemotherapeutic agent for gastric cancer; however, resistance limits its effectiveness. Investigation into the underlying mechanisms of paclitaxel resistance is urgently required. In the present study, a paclitaxel‑resistant gastric cancer cell line (MGC‑803R) was generated with a morphological phenotype of epithelial‑to‑mesenchymal transition (EMT) and increased expression levels of microRNA (miR)‑155‑5p. MGC‑803R cell‑derived exosomes were effectively taken up by paclitaxel‑sensitive MGC‑803S cells, which exhibited EMT and chemoresistance phenotypes. miR‑155‑5p was enriched in MGC‑803R‑exosomes and could be delivered into MGC‑803S cells. miR‑155‑5p overexpression in MGC‑803S cells via transfection with mimics resulted in similar phenotypic effects as treatment with MGC‑803R exosome and increased miR‑155‑5p content in MGC‑803S exosomes, which then capable of inducing the malignant phenotype in the sensitive cells. GATA binding protein 3 (GATA3) and tumor protein p53‑inducible nuclear protein 1 (TP53INP1) were identified as targets of miR‑155‑5p. Exosomal miR‑155‑5p inhibited these targets by directly targeting their 3' untranslated regions. Knockdown of miR‑155‑5p was observed to reverse the EMT and chemoresistant phenotypes of MGC‑803R cells, potentially via GATA3 and TP53INP1 upregulation, which inhibited MGC‑803R‑exosomes from inducing the malignant phenotype. These results demonstrated that exosomal delivery of miR‑155‑5p may induce EMT and chemoresistant phenotypes from paclitaxel‑resistant gastric cancer cells to the sensitive cells, which may be mediated by GATA3 and TP53INP1 suppression. Targeting miR‑155‑5p may thus be a promising strategy to overcome paclitaxel resistance in gastric cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.