ArticleCell death & disease2024
HMGB1 promotes mitochondrial transfer between hepatocellular carcinoma cells through RHOT1 and RAC1 under hypoxia.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 23 citations in OpenAlex.
- Sigma-1 receptor protects against renal ischemia-reperfusion injury by enhancing mitophagy via Rac1 regulation.Renal failure · 2026Article
- Platelet-derived mitochondrial transfer in cancer metastasis: mechanisms, functional consequences, and translational opportunities.Clinical & experimental metastasis · 2026Review
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Context-Dependent Functional Outcomes of Mitochondrial Transfer: A Donor-Recipient Perspective.Advanced biology · 2026Review
- Image feature embedding with a deep learning framework improves genome-wide association studies on dog endophenotypes.Science advances · 2026Article
- Mitochondria transfer: intercellular communication and tumor microenvironment dynamics.Cell communication and signaling : CCS · 2026Review
- Mobile Powerhouses: Mitochondria Transfer via Tunnelling Nanotubes in Brain Health and Neurodegenerative Diseases.The European journal of neuroscience · 2026Review
- From the energy factory to the intercellular communication medium: the emerging role of intercellular mitochondrial transfer and mitochondrial transplantation therapy in diabetes and diabetic complications.Journal of translational medicine · 2026Review
- Advances in mitochondrial-targeted colorectal cancer therapy: Mechanistic insights and clinical translation.iScience · 2026Review
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Mitochondrial transfer in cancer: mechanisms, immune evasion, and therapeutic opportunities.Genomics & informatics · 2026Review
- Mitochondrial transfer in the tumor microenvironment: a dynamic determinant of cancer plasticity, immune dysfunction, and therapeutic opportunity.Frontiers in immunology · 2026Review
- Mitochondrial transfer and mesenchymal stem cells in ophthalmology: current evidence and therapeutic implications.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Mitochondrial transfer: a new perspective on tumor-microenvironment crosstalk driving metastasis.Frontiers in immunology · 2026Review
- Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026Review
- Hypoxia-induced PYCR1 regulates glycolysis and histone lactylation to promote bladder cancer progression and metastasis via SLC6A14/Glutamine metabolism.Cancer biology & therapy · 2025Article
- Mechanisms of Mitochondrial Transfer Through TNTs: From Organelle Dynamics to Cellular Crosstalk.International journal of molecular sciences · 2025Review
- HMGB1 orchestrates tumor-osteoclast crosstalk to drive bone metastasis in hepatocellular carcinoma.Cell death & disease · 2025Article
- Inhibition of the HMGB1-RAGE Axis Attenuates Microglial Inflammation and Ameliorates Hypoxia-Induced Cognitive Impairment.International journal of molecular sciences · 2025Article
- MTFR2-Mediated Fission Drives Fatty Acid and Mitochondrial Co-Transfer from Hepatic Stellate Cells to Tumor Cells Fueling Oncogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondrial transfer plays an important role in various diseases, and many mitochondrial biological functions can be regulated by HMGB1. To explore the role of mitochondrial transfer in hepatocellular carcinoma (HCC) and its relationship with HMGB1, field emission scanning electron microscopy, immunofluorescence, and flow cytometry were used to detect the mitochondrial transfer between HCC cells. We found that mitochondrial transfer between HCC cells was confirmed using tunnel nanotubes (TNTs). The transfer of mitochondria from the highly invasive HCC cells to the less invasive HCC cells could enhance the migration and invasion ability of the latter. The hypoxic conditions increased the mitochondrial transfer between HCC cells. Then the mechanism was identified using co-immunoprecipitation, luciferase reporter assay, and chromatin immunoprecipitation. We found that RHOT1, a mitochondrial transport protein, promoted mitochondrial transfer and the migration and metastasis of HCC cells during this process. Under hypoxia, HMGB1 further regulated RHOT1 expression by increasing the expression of NFYA and NFYC subunits of the NF-Y complex. RAC1, a protein associated with TNTs formation, promoted mitochondrial transfer and HCC development. Besides, HMGB1 regulated RAC1 aggregation to the cell membrane under hypoxia. Finally, the changes and significance of related molecules in clinical samples of HCC were analyzed using bioinformatics and tissue microarray analyses. We found that HCC patients with high HMGB1, RHOT1, or RAC1 expression exhibited a relatively shorter overall survival period. In conclusion, under hypoxic conditions, HMGB1 promoted mitochondrial transfer and migration and invasion of HCC cells by increasing the expression of mitochondrial transport protein RHOT1 and TNTs formation-related protein RAC1.
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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.