ArticleJournal of cell communication and signaling2025
Extracellular vesicle-LncRNA HOTAIR modulates esophageal cancer chemoresistance and immune microenvironment via miR-375/CDH2 pathway.
Article in Journal of cell communication and signaling, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 papers.
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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
7 citing papers in PubMed.
- LncRNA DLGAP1-AS2 promotes ESCC progression and indicates unfavorable prognosis via the miR-101-3p/EZH2 axis.Discover oncology · 2026Article
- Tumor exosomes impact functional hallmarks of cancer.Cancer metastasis reviews · 2026Review
- The CeRNA role of HOTAIR: sponging MiRs to promote chemoresistance.Molecular biology reports · 2026Review
- EV-associated HOTAIR in cancer cell communication: a distance-aware review of functional transfer claims.Frontiers in cell and developmental biology · 2026Review
- The Interplay Between lncRNAs-microRNAs Network Dysregulation and Cellular Hallmarks of Thyroid Cancer.Cancers · 2025Review
- The role and targeting strategies of non-coding RNAs in immunotherapy resistance in oral squamous cell carcinoma.Frontiers in cell and developmental biology · 2025Review
- Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemoresistance and immune evasion remain significant barriers to effective esophageal cancer (EC) treatment. This study explores the mechanistic role of extracellular vesicles (EVs) delivering LncRNA HOTAIR in modulating these processes. Using transcriptomic profiling, LncRNA HOTAIR was identified as a critical factor in EC progression. Its interaction with miR-375 was examined via luciferase reporter assays and RNA immunoprecipitation. Paclitaxel-resistant EC cells were treated with EVs containing HOTAIR, and the functional impact on proliferation, migration, invasion, and immune response was assessed through in vitro and in vivo models. LncRNA HOTAIR in EVs enhanced paclitaxel resistance by suppressing miR-375 and increasing CDH2 expression. Furthermore, HOTAIR promoted immune escape by upregulating PD-L1, impairing T-cell-mediated cytotoxicity. These changes were validated in patient-derived EC models. This study demonstrates that EV-LncRNA HOTAIR mediates chemoresistance and immune evasion in EC by targeting the miR-375/CDH2 axis. These findings provide a foundation for novel therapeutic interventions targeting EV-HOTAIR.
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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.