ArticleJournal of hematology & oncology2018
Cell adhesion-mediated mitochondria transfer contributes to mesenchymal stem cell-induced chemoresistance on T cell acute lymphoblastic leukemia cells.
Article in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers.
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Who cites it
161 citing papers in PubMed, 263 citations in OpenAlex.
- Platelet-derived mitochondrial transfer in cancer metastasis: mechanisms, functional consequences, and translational opportunities.Clinical & experimental metastasis · 2026Review
- Photopolymerizable placenta-derived ECM hydrogel enhances hUC-MSC-mediated wound healing via coordinated immunomodulation and angiogenesis.Materials today. Bio · 2026Article
- Mitochondrial transfer between tumor and immune cells: a nexus of metabolic adaptation and immune dysfunction.Biomarker research · 2026Review
- Mitochondria transfer in glioblastoma.Neuro-oncology · 2026Review
- Mitochondrial Transfer in the Tumor Microenvironment.Cancer science · 2026Review
- Mitochondria transfer: intercellular communication and tumor microenvironment dynamics.Cell communication and signaling : CCS · 2026Review
- Breaking cellular boundaries: molecular mechanisms of tunneling nanotube formation and fusion.Biochemical Society transactions · 2026Review
- Mitochondrial transfer to granulocytic myeloid-derived suppressor cells augments immunosuppressive activity.Cell reports · 2026Article
- Review
- Transfer of Damaged Mitochondria from Cancer Cells to Cancer-Associated Fibroblasts Promotes Tyrosine Kinase Inhibitor Tolerance in EGFR-Mutant Lung Cancer.Cancer research · 2026Article
- Mitochondrial transfer in the HSC-HCC-macrophage network shapes hepatocellular carcinoma progression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- MUC1 promotes NSCLC progression by regulating ICAM-1-mediated mitochondria transfer from tCAFs to cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Targeting mitochondrial homeostasis as a cancer treatment strategy: current status and future prospects.Molecular cancer · 2026Review
- Recent Advances in Mitochondrial Transplantation for Ischemic Stroke: A Review of in Vitro and in Vivo Studies.Translational stroke research · 2026Review
- Mitochondrial transfer in cancer: mechanisms, immune evasion, and therapeutic opportunities.Genomics & informatics · 2026Review
- Mitochondrial transfer as a driver of immune microenvironment remodeling.Frontiers in immunology · 2026Review
- The application of nanotechnology in regulating mitochondrial function in tumor microenvironment for cancer therapy.Theranostics · 2026Review
- Mesenchymal Stromal Cells: Bridging the Gaps in Hematologic Disease Therapy.Stem cell reviews and reports · 2026Review
- Isoliensinine inhibits mitophagy and sensitizes T cell malignancies for STING-mediated NK clearance.Acta pharmacologica Sinica · 2026Article
101 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDespite the high cure rate of T cell acute lymphoblastic leukemia (T-ALL), drug resistance to chemotherapy remains a significant clinical problem. Bone marrow mesenchymal stem cells (MSCs) protect leukemic cells from chemotherapy, but the underlying mechanisms are poorly understood. In this study, we aimed to uncover the mechanism of MSC-induced chemoresistance in T-ALL cells, thus providing a promising clinical therapy target.
methodsCell viability was determined using the viability assay kit CCK-8. The mitochondrial ROS levels were detected using the fluorescent probe MitoSOX™ Red, and fluorescence intensity was measured by flow cytometry. In vitro, MSCs and Jurkat cells were cocultured. MSCs were labeled with green fluorescent protein (GFP), and Jurkat cells were labeled with the mitochondria-specific dye MitoTracker Red. Bidirectional mitochondrial transfer was detected by flow cytometry and confocal microscopy. The mechanism of mitochondria transfer was analyzed by inhibitor assays. Transcripts related to Jurkat cell/MSC adhesion in the coculture system were assessed by qRT-PCR. After treatment with a neutralizing antibody against a key adhesion molecule, mitochondria transfer from Jurkat cells to MSCs was again detected by flow cytometry and confocal microscopy. Finally, we verified our findings using human primary T-ALL cells cocultured with MSCs.
resultsChemotherapeutic drugs caused intracellular oxidative stress in Jurkat cells. Jurkat cells transfer mitochondria to MSCs but receive few mitochondria from MSCs, resulting in chemoresistance. This process of mitochondria transfer is mediated by tunneling nanotubes, which are protrusions that extend from the cell membrane . Moreover, we found that most Jurkat cells adhered to MSCs in the coculture system, which was mediated by the adhesion molecule ICAM-1. Treatment with a neutralizing antibody against ICAM-1 led to a decreased number of adhering Jurkat cells, decreased mitochondria transfer, and increased chemotherapy-induced cell death.
conclusionsWe show evidence that mitochondria transfer from Jurkat cells to MSCs, which is mediated by cell adhesion, may be a potential therapeutic target for T-ALL treatment.
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