ArticleCell cycle (Georgetown, Tex.)2022
Lymphoma cell-derived extracellular vesicles inhibit autophagy and apoptosis to promote lymphoma cell growth via the microRNA-106a/Beclin1 axis.
Article in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Extracellular Vesicles in B-Cell Non-Hodgkin Lymphomas: Pathogenesis, Therapeutic Implications, and Biomarker Potential.Biomedicines · 2026Review
- An update on extracellular vesicles in hematologic disorders: molecular mediators, clinical biomarkers, and emerging therapeutics.Molecular biology reports · 2025Review
- MiR-106a targets ATG7 to inhibit autophagy and angiogenesis after myocardial infarction.Animal models and experimental medicine · 2024Article
- Menthol induces extracellular vesicle regulation of apoptosis via ATG3 and caspase-3 in acute leukemic cells.Heliyon · 2024Article
- Deciphering pancreatic neuroendocrine tumors: Unveiling through circulating small extracellular vesicles.Heliyon · 2024Article
- The Role of Extracellular Vesicles in the Pathogenesis of Hematological Malignancies: Interaction with Tumor Microenvironment; a Potential Biomarker and Targeted Therapy.Biomolecules · 2023Review
- Anti-inflammation is an important way that Qingre-Huazhuo-Jiangsuan recipe treats acute gouty arthritis.Frontiers in pharmacology · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lymphoma is a common malignant tumor globally. Tumor-derived extracellular vesicles (Evs) participate in genetic information exchange between tumor cells. We investigated the role and mechanism of human Burkitt lymphoma cells Raji-derived Evs (Raji-Evs) in lymphoma cells. Effects of Evs on lymphoma cell proliferation, invasion, autophagy, and apoptosis were assessed using Cell Counting Kit-8 method, Transwell assay, laser confocal microscopy, Western blotting, and flow cytometry. microRNA (miR)-106a expression in lymphoma cells was determined using reverse transcription-quantitative polymerase chain reaction and then downregulated in Raji cells and then Evs were isolated (Evs-in-miR-106a) to evaluate its role in lymphoma cell growth. The binding relationship between miR-106a and Beclin1 was verified using RNA pull-down and dual-luciferase assays. Beclin1 was overexpressed in SU-DHL-4 and Farage cells and SU-DHL-4 cell autophagy and apoptosis were detected. The levels of miR-106a and Beclin1 in SU-DHL-4 cells were detected after adding autophagy inhibitors. The tumorigenicity assay in nude mice was performed to validate the effects of Raji-Evs
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Registered trials
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