ArticleThe Journal of biological chemistry2013
Essential role of class II phosphatidylinositol-3-kinase-C2α in sphingosine 1-phosphate receptor-1-mediated signaling and migration in endothelial cells.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 66 citations in OpenAlex.
- Novel role of the class II α-isoform of phosphatidylinositol 3-kinase in hepatocellular carcinoma: suppressing metastasis by targeting Wnt/β-catenin signaling via inhibiting phosphorylation of LRP6.Cancer cell international · 2026Article
- Inavolisib-based Combination Therapy for the Treatment of PIK3CAMutated HR+/HER2- Breast Cancer: An Overview.Mini reviews in medicinal chemistry · 2026Review
- Highlighting the Importance of Signaling Pathways and Immunohistochemistry Features in HCC: A Case Report and Literature Review.Reports (MDPI) · 2025Article
- Inactivation of PI3K-C2α deregulates cell death pathways and sensitizes to endotoxic shock.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CARM1 regulates tubulin autoregulation through PI3KC2α R175 methylation.Cell communication and signaling : CCS · 2025Article
- Structural Basis for Highly Selective Class II Alpha Phosphoinositide-3-Kinase Inhibition.Journal of medicinal chemistry · 2023Article
- Decompression Mechanism of Radish Seed in Prehypertension Rats through Integration of Transcriptomics and Metabolomics Methods.Evidence-based complementary and alternative medicine : eCAM · 2023Article
- Structural basis of phosphatidylinositol 3-kinase C2α function.Nature structural & molecular biology · 2022Article
- PI3K Isoforms in Vascular Biology, A Focus on the Vascular System-Immune Response Connection.Current topics in microbiology and immunology · 2022Article
- The Role of Phosphatidylinositol 3-Kinase Catalytic Subunit Type 3 in the Pathogenesis of Human Cancer.International journal of molecular sciences · 2021Review
- Class II phosphatidylinositol 3-kinase isoforms in vesicular trafficking.Biochemical Society transactions · 2021Review
- Class II phosphatidylinositol 3-kinase-C2α is essential for Notch signaling by regulating the endocytosis of γ-secretase in endothelial cells.Scientific reports · 2021Article
- Evaluation of active Rac1 levels in cancer cells: A case of misleading conclusions from immunofluorescence analysis.The Journal of biological chemistry · 2020Article
- TGFβ receptor endocytosis and Smad signaling require synaptojanin1, PI3K-C2α-, and INPP4B-mediated phosphoinositide conversions.Molecular biology of the cell · 2020Article
- MicroRNA-4316 inhibits gastric cancer proliferation and migration via directly targeting VEGF-A.Cancer cell international · 2020Article
- PI3K isoforms in cell signalling and vesicle trafficking.Nature reviews. Molecular cell biology · 2019Review
- Class II PI3Ks at the Intersection between Signal Transduction and Membrane Trafficking.Biomolecules · 2019Review
- The class II phosphoinositide 3-kinases PI3K-C2α and PI3K-C2β differentially regulate clathrin-dependent pinocytosis in human vascular endothelial cells.The journal of physiological sciences : JPS · 2019Article
- Revisiting PI3-kinase signalling in angiogenesis.Vascular biology (Bristol, England) · 2019Review
- Multi-hierarchical profiling the structure-activity relationships of engineered nanomaterials at nano-bio interfaces.Nature communications · 2018Article
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7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphatidylinositol (PtdIns) 3-kinase (PI3K) family regulates diverse cellular processes, including cell proliferation, migration, and vesicular trafficking, through catalyzing 3'-phosphorylation of phosphoinositides. In contrast to class I PI3Ks, including p110α and p110β, functional roles of class II PI3Ks, comprising PI3K-C2α, PI3K-C2β, and PI3K-C2γ, are little understood. The lysophospholipid mediator sphingosine 1-phosphate (S1P) plays the important roles in regulating vascular functions, including vascular formation and barrier integrity, via the G-protein-coupled receptors S1P(1-3). We studied the roles of PI3K-C2α in S1P-induced endothelial cell (EC) migration and tube formation. S1P stimulated cell migration and activation of Akt, ERK, and Rac1, the latter of which acts as a signaling molecule essential for cell migration and tube formation, via S1P(1) in ECs. Knockdown of either PI3K-C2α or class I p110β markedly inhibited S1P-induced migration, lamellipodium formation, and tube formation, whereas that of p110α or Vps34 did not. Only p110β was necessary for S1P-iduced Akt activation, but both PI3K-C2α and p110β were required for Rac1 activation. FRET imaging showed that S1P induced Rac1 activation in both the plasma membrane and PtdIns 3-phosphate (PtdIns(3)P)-enriched endosomes. Knockdown of PI3K-C2α but not p110β markedly reduced PtdIns(3)P-enriched endosomes and suppressed endosomal Rac1 activation. Also, knockdown of PI3K-C2α but not p110β suppressed S1P-induced S1P(1) internalization into PtdIns(3)P-enriched endosomes. Finally, pharmacological inhibition of endocytosis suppressed S1P-induced S1P(1) internalization, Rac1 activation, migration, and tube formation. These observations indicate that PI3K-C2α plays the crucial role in S1P(1) internalization into the intracellular vesicular compartment, Rac1 activation on endosomes, and thereby migration through regulating vesicular trafficking in ECs.
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