ArticleCell stress & chaperones2015
LRIG1 inhibits hypoxia-induced vasculogenic mimicry formation via suppression of the EGFR/PI3K/AKT pathway and epithelial-to-mesenchymal transition in human glioma SHG-44 cells.
Article in Cell stress & chaperones, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- Leucine-rich repeats and immunoglobulin-like domains 3 suppresses hypoxia-induced vasculogenic mimicry in glioma by promoting the ubiquitination and degradation of Snail2.Cell stress & chaperones · 2026Article
- Transcriptomic-Driven Drug Repurposing Reveals SP600125 as a Promising Drug Candidate for the Treatment of Glial-Mesenchymal Transition in Glioblastoma.International journal of molecular sciences · 2025Article
- The Roles of RNA-Binding Proteins in Vasculogenic Mimicry Regulation in Glioblastoma.International journal of molecular sciences · 2025Review
- TJP1 promotes vascular mimicry in bladder cancer by facilitating VEGFA expression and transcriptional activity through TWIST1.Translational oncology · 2023Article
- L1CAM promotes vasculogenic mimicry formation by miR-143-3p-induced expression of hexokinase 2 in glioma.Molecular oncology · 2023Article
- The Dual Effects of Exosomes on Glioma: A Comprehensive Review.Journal of Cancer · 2023Review
- Glioblastoma-Specific Strategies of Vascularization: Implications in Anti-Angiogenic Therapy Resistance.Journal of personalized medicine · 2022Review
- m6A methylated EphA2 and VEGFA through IGF2BP2/3 regulation promotes vasculogenic mimicry in colorectal cancer via PI3K/AKT and ERK1/2 signaling.Cell death & disease · 2022Article
- Tumor Vessels Fuel the Fire in Glioblastoma.International journal of molecular sciences · 2021Review
- Article
- Selective exosome exclusion of miR-375 by glioma cells promotes glioma progression by activating the CTGF-EGFR pathway.Journal of experimental & clinical cancer research : CR · 2021Article
- PI3K/AKT signaling pathway as a critical regulator of Cisplatin response in tumor cells.Oncology research · 2021Review
- Down-regulating NEAT1 inhibited the viability and vasculogenic mimicry formation of sinonasal squamous cell carcinoma cells via miR-195-5p/VEGFA axis.Bioscience reports · 2020Article
- Vascular mimicry: changing the therapeutic paradigms in cancer.Molecular biology reports · 2020Review
- Celastrol Suppresses Glioma Vasculogenic Mimicry Formation and Angiogenesis by Blocking the PI3K/Akt/mTOR Signaling Pathway.Frontiers in pharmacology · 2020Article
- Advances and Prospects of Vasculogenic Mimicry in Glioma: A Potential New Therapeutic Target?OncoTargets and therapy · 2020Review
- Article
- LRIG1 acts as a critical regulator of melanoma cell invasion, migration, and vasculogenic mimicry upon hypoxia by regulating EGFR/ERK-triggered epithelial-mesenchymal transition.Bioscience reports · 2019Article
- Regulation Networks Driving Vasculogenic Mimicry in Solid Tumors.Frontiers in oncology · 2019Review
- Downregulation of microRNA-4295 enhances cisplatin-induced gastric cancer cell apoptosis through the EGFR/PI3K/Akt signaling pathway by targeting LRIG1.International journal of oncology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a pan-negative regulator of the epidermal growth factor receptor (EGFR) signaling pathway. The aim of this study was to investigate the underlying mechanism of LRIG1 in the regulation of vasculogenic mimicry (VM) formation in glioma cells. We constructed an enhanced green fluorescent protein plasmid (pEGFP) system, pEGFP-C1-LRIG1, for overexpression of LRIG1, and transfected it into human glioma cell line SHG-44. Under hypoxic conditions induced by CoCl2, we investigated the effects of LRIG1 overexpression on VM formation and VM-dependent malignant behaviors including migration, invasion, and proliferation. Additionally, we explored the effects of LRIG1 on the expression levels of major components of the EGFR/PI3K/AKT pathway as well as E-cadherin and vimentin. We found that LRIG1 overexpression is able to inhibit hypoxia-induced VM formation, migration, invasion, and proliferation. Furthermore, LRIG1 overexpression counteracts hypoxia-induced increase in the expression of phosphorylated EGFR (pEGFR), PI3K (pPI3K), and AKT (pAKT) and reverts hypoxia-induced alteration in E-cadherin and vimentin expression levels. In LRIG1 knockdown SHG-44 cells, however, hypoxia-induced VM formation and alteration in E-cadherin and vimentin expression levels were exacerbated. These results suggest that the inhibitory effects of LRIG1 are most likely mediated by suppression of the EGFR/PI3K/AKT pathway and epithelial-mesenchymal transition (EMT) process. Our findings provide compelling evidence implicating LRIG1 in glioma pathophysiology, suggesting that gene therapy using LRIG1 may serve as a treatment for this disease.
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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.