ArticleScientific reports2023
mTORC2 interactome and localization determine aggressiveness of high-grade glioma cells through association with gelsolin.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Pdcd4-Rictor interaction suppresses mTORC2-PFKFB3 axis and tumorigenesis in NSCLC.Neoplasia (New York, N.Y.) · 2026Article
- A human telomerase reverse transcriptase-derived peptide GV1001 rescues neurodegeneration in a mouse model of Alzheimer disease.Experimental & molecular medicine · 2026Article
- Pharmacological Ascorbate Restrains Epithelial-Mesenchymal Transition and Invasion in Glioblastoma Cells via Extracellular HInternational journal of molecular sciences · 2026Article
- Pdcd4-Rictor Interaction Suppresses PFKFB3 to inhibit Tumorigenesis.Research square · 2026Article
- PTBP1 supports mouse spermatogenesis by facilitating cytoskeletal organization through the mTORC2-PKCα pathway in Sertoli cells.Communications biology · 2026Article
- Inhibition of TRAF3IP2 Modulates NAMPT and NAD Metabolism in Glioblastoma.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- A Bibenzyl fromAntioxidants (Basel, Switzerland) · 2025Article
- Phenotypic rescue via mTOR inhibition in neuron-specific Pten knockout mice reveals AKT and mTORC1-site specific changes.Molecular psychiatry · 2025Article
- Cinnamaldehyde impacts key cellular signaling pathways for induction of programmed cell death in high-grade and low-grade human glioma cells.BMC research notes · 2025Article
- Review
- The mTORC2 signaling network: targets and cross-talks.The Biochemical journal · 2024Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
mTOR complex 2 (mTORC2) has been implicated as a key regulator of glioblastoma cell migration. However, the roles of mTORC2 in the migrational control process have not been entirely elucidated. Here, we elaborate that active mTORC2 is crucial for GBM cell motility. Inhibition of mTORC2 impaired cell movement and negatively affected microfilament and microtubule functions. We also aimed to characterize important players involved in the regulation of cell migration and other mTORC2-mediated cellular processes in GBM cells. Therefore, we quantitatively characterized the alteration of the mTORC2 interactome under selective conditions using affinity purification-mass spectrometry in glioblastoma. We demonstrated that changes in cell migration ability specifically altered mTORC2-associated proteins. GSN was identified as one of the most dynamic proteins. The mTORC2-GSN linkage was mostly highlighted in high-grade glioma cells, connecting functional mTORC2 to multiple proteins responsible for directional cell movement in GBM. Loss of GSN disconnected mTORC2 from numerous cytoskeletal proteins and affected the membrane localization of mTORC2. In addition, we reported 86 stable mTORC2-interacting proteins involved in diverse molecular functions, predominantly cytoskeletal remodeling, in GBM. Our findings might help expand future opportunities for predicting the highly migratory phenotype of brain cancers in clinical investigations.
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