ArticlePloS one2019
Glycogen synthase kinase 3-β inhibition induces lymphangiogenesis through β-catenin-dependent and mTOR-independent pathways.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Pharmacological intervention of Chinese medicine via regulating ferroptosis in gastric cancer.Chinese medicine · 2026Review
- Exosomal miR-224-3p promotes lymphangiogenesis and lymph node metastasis by targeting GSK3B in gastric cancer.Oncology research · 2025Article
- Elucidation of the GSK3α Structure Informs the Design of Novel, Paralog-Selective Inhibitors.ACS chemical neuroscience · 2023Article
- Exosomal miR-10527-5p Inhibits Migration, Invasion, Lymphangiogenesis and Lymphatic Metastasis by Affecting Wnt/β-Catenin Signaling via Rab10 in Esophageal Squamous Cell Carcinoma.International journal of nanomedicine · 2023Article
- Article
- Extracellular Matrix Stiffness: New Areas Affecting Cell Metabolism.Frontiers in oncology · 2021Review
- FK506 induces lung lymphatic endothelial cell senescence and downregulates LYVE-1 expression, with associated decreased hyaluronan uptake.Molecular medicine (Cambridge, Mass.) · 2020Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Lymphatic vessels play an important role in health and in disease. In this study, we evaluated the effects of GSK3-β inhibition on lung lymphatic endothelial cells in vitro. Pharmacological inhibition and silencing of GSK3-β resulted in increased lymphangiogenesis of lung lymphatic endothelial cells. To investigate mechanisms of GSK3-β-mediated lymphangiogenesis, we interrogated the mammalian/mechanistic target of rapamycin pathway and found that inhibition of GSK3-β resulted in PTEN activation and subsequent decreased activation of AKT, leading to decreased p-P70S6kinase levels, indicating inhibition of the mTOR pathway. In addition, consistent with a negative role of GSK3-β in β-catenin stability through protein phosphorylation, we found that GSK3-β inhibition resulted in an increase in β-catenin levels. Simultaneous silencing of β-catenin and inhibition of GSK3-β demonstrated that β-catenin is required for GSK3-β-induced lymphangiogenesis.
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