ArticleCell biology and toxicology2023
Extracellular vesicles derived from paclitaxel-sensitive nasopharyngeal carcinoma cells deliver miR-183-5p and impart paclitaxel sensitivity through a mechanism involving P-gp.
Article in Cell biology and toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 9 citations in OpenAlex.
- The striking divergence of ABCB1 mRNA expression and P-glycoprotein protein levels in M1 and M2 macrophages associates with the microRNA miR-21-3p, a regulator of "RNA binding protein, mRNA processing factor".Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Extracellular Vesicles: A Multidimensional Role in the Occurrence and Development of Nasopharyngeal Carcinoma.Biomolecules · 2026Review
- MiRNAs: main players of cancer drug resistance target ABC transporters.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Review
- Bioinformatics and Experimental Study Revealed LINC00982/ miR-183-5p/ABCA8 Axis Suppresses LUAD Progression.Current cancer drug targets · 2024Article
- Intercellular transfer of multidrug resistance mediated by extracellular vesicles.Cancer drug resistance (Alhambra, Calif.) · 2024Review
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4 authors at 1 institution in 1 country.
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Abstract
Paclitaxel treatment has been applied for late-stage nasopharyngeal carcinoma (NPC), but therapy failure usually occurs due to paclitaxel resistance. Besides, microRNAs (miRs) delivered by extracellular vesicles (EVs) have been demonstrated as promising biomarkers affecting cancer development. Our work clarified the role of bioinformatically predicted miR-183-5p, which could be delivered by EVs, in the paclitaxel resistance of NPC. Downstream targets of miR-183-5p were predicted in publicly available databases, followed by GO enrichment analysis. A confirmatory dual-luciferase reporter assay determined the targeting relationship between miR-183-5p and P-glycoprotein (P-gp). The shuttling of extracellular miR-183-5p was identified by immunofluorescence. EVs transferred miR-183-5p from paclitaxel-sensitive NPC cells to paclitaxel-resistant NPC cells. Furthermore, overexpression of miR-183-5p and under-expression of P-gp occurred in clinical samples and cells of NPC. High expression of miR-183-5p corresponded to better survival of paclitaxel-treated patients. The effects of manipulated expression of miR-183-5p on NPC cell activities, tumor growth, and paclitaxel resistance were investigated in vitro and in vivo. Its effect was achieved through negatively regulating drug transporters P-gp. Ectopically expressed miR-183-5p enhanced the cancer-suppressive effects of paclitaxel by targeting P-gp, corresponding to diminished cell viability and tumor growth. Taken together, this work goes to elucidate the mechanical actions of miR-183-5p delivered by EVs and its significant contribution towards paclitaxel sensitivity to NPC. 1. This study provides mechanistic insight into the role of miR-183-5p-containing EVs in NPC. 2. The intercellular transportation of miR-183-5p is mediated by EVs in NPC. 3. Overexpressing miR-183-5p facilitates the anti-tumor effects of paclitaxel in NPC. 4. miR-183-5p suppresses paclitaxel resistance of NPC cells by inhibiting P-gp.
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