ArticleNature communications2018
Arf6-driven cell invasion is intrinsically linked to TRAK1-mediated mitochondrial anterograde trafficking to avoid oxidative catastrophe.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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Who cites it
44 citing papers in PubMed, 82 citations in OpenAlex.
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- Identification and validation of ARF6 for a potential prognostic biomarker of acute myeloid leukemia.Cancer cell international · 2025Article
- Extracellular matrix dynamics in tumor immunoregulation: from tumor microenvironment to immunotherapy.Journal of hematology & oncology · 2025Review
- CML With Mutant ASXL1 Showed Decreased Sensitivity to TKI Treatment via Upregulation of the ALOX5-BLTR Signaling Pathway.Cancer science · 2025Article
- Amniotic epithelial Cell microvesicles uptake inhibits PBMCs and Jurkat cells activation by inducing mitochondria-dependent apoptosis.iScience · 2025Article
- p53 ensures the normal behavior and modification of G1/S-specific histone H3.1 in the nucleus.Life science alliance · 2024Article
- Tumour-intrinsic endomembrane trafficking by ARF6 shapes an immunosuppressive microenvironment that drives melanomagenesis and response to checkpoint blockade therapy.Nature communications · 2024Article
- In vivo CRISPR screening directly targeting testicular cells.Cell genomics · 2024Article
- The C. elegans anchor cell: A model to elucidate mechanisms underlying invasion through basement membrane.Seminars in cell & developmental biology · 2024Review
- Confinement primes cells for faster migration by polarizing active mitochondria.Nanoscale advances · 2023Article
- Arf6 as a therapeutic target: Structure, mechanism, and inhibitors.Acta pharmaceutica Sinica. B · 2023Review
- Neutrophils in Cancer and Potential Therapeutic Strategies Using Neutrophil-Derived Exosomes.Vaccines · 2023Review
- KRAS, MYC, and ARF6: inseparable relationships cooperatively promote cancer malignancy and immune evasion.Cell communication and signaling : CCS · 2023Review
- Combination Cancer Treatment: Using Engineered DNAzyme Molecular Machines for Dynamic Inter- and Intracellular Regulation.Angewandte Chemie (International ed. in English) · 2022Article
- A Protumorigenic mDia2-MIRO1 Axis Controls Mitochondrial Positioning and Function in Cancer-Associated Fibroblasts.Cancer research · 2022Article
- Glaesserella parasuis serotype 5 breaches the porcine respiratory epithelial barrier by inducing autophagy and blocking the cell membrane Claudin-1 replenishment.PLoS pathogens · 2022Article
- Mitochondrial adaptation in cancer drug resistance: prevalence, mechanisms, and management.Journal of hematology & oncology · 2022Review
- Mitochondrial transfer/transplantation: an emerging therapeutic approach for multiple diseases.Cell & bioscience · 2022Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondria dynamically alter their subcellular localization during cell movement, although the underlying mechanisms remain largely elusive. The small GTPase Arf6 and its signaling pathway involving AMAP1 promote cell invasion via integrin recycling. Here we show that the Arf6-AMAP1 pathway promote the anterograde trafficking of mitochondria. Blocking the Arf6-based pathway causes mitochondrial aggregation near the microtubule-organizing center, and subsequently induces detrimental reactive oxygen species (ROS) production, likely via a mitochondrial ROS-induced ROS release-like mechanism. The Arf6-based pathway promotes the localization of ILK to focal adhesions to block RhoT1-TRAK2 association, which controls mitochondrial retrograde trafficking. Blockade of the RhoT1-TRAK1 machinery, rather than RhoT1-TRAK2, impairs cell invasion, but not two-dimensional random cell migration. Weakly or non-invasive cells do not notably express TRAK proteins, whereas they clearly express their mRNAs. Our results identified a novel association between cell movement and mitochondrial dynamics, which is specific to invasion and is necessary for avoiding detrimental ROS production.
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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.