ArticleBioactive materials2024
Tumor-derived apoptotic extracellular vesicle-mediated intercellular communication promotes metastasis and stemness of lung adenocarcinoma.
Article in Bioactive materials, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 16 citations in OpenAlex.
- CCT2 enhances c-Myc stabilization to drive tumor progression and chemoresistance in head and neck squamous cell carcinoma.Genes & diseases · 2026Article
- The CRABP2-MDK Signaling Axis Promotes Lung Adenocarcinoma (LUAD) Progression and Highlights Prognostic Biomarkers.Molecular carcinogenesis · 2026Article
- Engineered extracellular vesicles for combinatorial cancer therapy and imaging.Acta pharmaceutica Sinica. B · 2026Review
- EBF3 suppresses lung adenocarcinoma progression and immune evasion via transcriptional repression of CCL24.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Apoptotic extracellular vesicles act as master regulators of the bone healing niche.Journal of nanobiotechnology · 2026Review
- Dying cells as architects of the stem cell niche: a conserved mechanism driving tissue regeneration and tumor therapy resistance.Cell communication and signaling : CCS · 2026Review
- Apoptotic vesicles in cancer: research progress in physiology and therapy.Cell communication and signaling : CCS · 2026Review
- Apoptotic vesicles: from biological characteristics to clinical translational prospects.Journal of translational medicine · 2026Review
- Neuroprotective effects of Berberine-loaded BMSCs-apoptotic extracellular vesicles on retinal ganglion cells: therapeutic potential for glaucomatous injury.Journal of nanobiotechnology · 2025Article
- Selective EV Protein Sorting and Pathway Perturbation in AML Upon Synergistic FLT3 and Hedgehog Pathway Inhibition.Journal of extracellular vesicles · 2025Article
- Chemotherapy reprograms miRNA expression profiles in apoptotic extracellular vesicles from medulloblastoma cells, regulating pro- and anti-proliferative effects on recipient drug-naïve cells.Cell communication and signaling : CCS · 2025Article
- TNFAIP2 promotes NF-κB signaling mediate lymph node metastasis of oral squamous cell carcinoma by protecting IKKβ from ubiquitin proteasome degradation.Cell communication and signaling : CCS · 2025Article
- Review
- Rapid and unbiased enrichment of extracellular vesicles via a meticulously engineered peptide.Bioactive materials · 2025Article
- ApoBDs: a paradigm shift from cellular debris to therapeutic vehicles.Frontiers in endocrinology · 2025Review
- Sepsis-driven metabolic reprogramming shapes cancer immunotherapy efficacy, metastatic potential, and drug sensitivity.Frontiers in immunology · 2025Review
- Apoptotic extracellular vesicles: emerging biomarkers for cancer and neurodegenerative disease diagnostics.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis has long been recognized as a significant mechanism for inhibiting tumor formation, and a plethora of stimuli can induce apoptosis during the progression and treatment of tumors. Moreover, tumor-derived apoptotic extracellular vesicles (apoEVs) are inevitably phagocytosed by live tumor cells, promoting tumor heterogeneity. Understanding the mechanism by which apoEVs regulate tumor cells is imperative for enhancing our knowledge of tumor metastasis and recurrence. Herein, we conducted a series of in vivo and in vitro experiments, and we report that tumor-derived apoEVs promoted lung adenocarcinoma (LUAD) metastasis, self-renewal and chemoresistance. Mechanistically, we demonstrated that apoEVs facilitated tumor metastasis and stemness by initiating the epithelial-mesenchymal transition program and upregulating the transcription of the stem cell factor SOX2. In addition, we found that ALDH1A1, which was transported by apoEVs, activated the NF-κB signaling pathway by increasing aldehyde dehydrogenase enzyme activity in recipient tumor cells. Furthermore, targeting apoEVs-ALDH1A1 significantly abrogated these effects. Collectively, our findings elucidate a novel mechanism of apoEV-dependent intercellular communication between apoptotic tumor cells and live tumor cells that promotes the formation of cancer stem cell-like populations, and these findings reveal that apoEVs-ALDH1A1 may be a potential therapeutic target and biomarker for LUAD metastasis and recurrence.
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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 Socratic graph.