ArticleCancer science2025
Engineered EVs-Mediated miR-222 Targeting PTEN/FN1 Axis Reverses Anthracycline Resistance in HER2-Negative Breast Cancer.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Exercise-responsive microRNA networks and extracellular vesicle-mediated microRNA signaling in breast cancer: linking tumor signaling, systemic crosstalk, and clinical relevance.Frontiers in oncology · 2026Review
- Engineered EVs-Mediated miR-222 Targeting PTEN/FN1 Axis Reverses Anthracycline Resistance in HER2-Negative Breast Cancer.Cancer science · 2025Article
- Functional foods and exercise in breast cancer: epigenetic modulation, chemotherapy tolerance, and fatigue management.Frontiers in nutrition · 2025Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Anthracycline resistance represents a critical therapeutic challenge in breast cancer treatment, wherein alterations in the tumor immune microenvironment and enhanced cellular resistance mechanisms facilitate chemoresistance progression. Transcriptome analysis of 142 HER2-negative breast cancer patients undergoing anthracycline-based chemotherapy revealed four distinct tumor-infiltrating cell subtypes, with subtype D exhibiting elevated M1 macrophage infiltration and superior prognostic outcomes. Differential expression analysis identified miR-222 as the predominantly upregulated microRNA in adriamycin-resistant cells, while Tandem Mass Tag mass spectrometry-based quantitative analysis elucidated PTEN as its direct target and FN1 as a crucial downstream mediator. Engineered extracellular vesicles (EVs) carrying a miR-222 inhibitor were developed to reverse adriamycin resistance via PTEN/FN1 signaling modulation. Molecular docking analysis found specific PTEN-FN1 protein interactions characterized by stable hydrogen bonds at ARG142-ASP23 and ARG15-GLU95. In xenograft models, EVs-mediated delivery of the miR-222 inhibitor significantly attenuated MCF-7/ADR tumor progression through miR-222 suppression and PTEN restoration, with concordant molecular alterations observed in serum-derived EVs. Our findings establish a novel mechanism of EVs-mediated drug resistance through the microRNA-222/PTEN/FN1 axis and present Engineered EVs as a promising therapeutic strategy for anthracycline resistance in breast cancer, while highlighting circulating EVs profiles as potential treatment monitoring biomarkers.
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Registered trials
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.