ArticleCell death & disease2023
SOX2 promotes vasculogenic mimicry by accelerating glycolysis via the lncRNA AC005392.2-GLUT1 axis in colorectal cancer.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Review
- Long non-coding RNAs in colorectal cancer: shaping the tumour microenvironment and advancing precision oncology.Nature reviews. Gastroenterology & hepatology · 2026Review
- Glucose Transporter 1 in Health and Disease.MedComm · 2026Review
- SAP18 drives vasculogenic mimicry in esophageal squamous cell carcinoma: a machine learning and multi-omics investigation.NPJ precision oncology · 2026Article
- PKM2 Lactylation Promotes Colorectal Cancer Vasculogenic Mimicry and Bevacizumab Resistance by Facilitating FOSL1 Super-enhancer Formation.Cancer research · 2026Article
- Direct targeting of GLUT1 in cancer: A decade of inhibitor discovery and medicinal chemistry insights.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- Integrative Analysis Identified an Eight-Gene Risk Signature Linked to CDK7 and Explored Its Association with HCC Progression via RelA Phosphorylation.Oncology research · 2026Article
- High Glycolysis and Lipid Metabolism Status Predicts Poor Prognosis in Colorectal Cancer Patients.Current molecular medicine · 2026Article
- Long non-coding RNAs in cancer glycolysis and metabolism: mechanisms and translational opportunities.Cell death & disease · 2025Review
- LBX2-AS1 in acceleration of glycolysis and cancer angiogenesis via miR-491-5p/MDK signaling axis in colorectal cancer: an experimental study.Annals of medicine · 2025Article
- Development and validation of a nomogram comprising GLUT1 and clinical characteristics for predicting overall survival in intrahepatic cholangiocarcinoma.Translational cancer research · 2025Article
- Murine Cell Line Models for Vascular Mimicry: The Role of YAP/TAZ Signaling.International journal of molecular sciences · 2025Article
- Glucose Metabolic Reprogramming in Colorectal Cancer: From Mechanisms to Targeted Therapy Approaches.Cancer medicine · 2025Review
- Review
- X-Linked Gene Dosage and SOX2 Act as Key Roadblocks for Human Germ Cell Specification in Klinefelter Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- TRMT10A regulates tRNA-ArgCCT mCell death & disease · 2025Article
- Transplantation of gastric epithelial mitochondria into human gastric cancer cells inhibits tumor growth and enhances chemosensitivity by reducing cancer stemness and modulating gastric cancer metabolism.Stem cell research & therapy · 2025Article
- Exploring the Link Between Noncoding RNAs and Glycolysis in Colorectal Cancer.Journal of cellular and molecular medicine · 2025Review
- Restoration of angiogenic capacity in senescent endothelial cells by a pharmacological reprogramming approach.PloS one · 2025Article
- The vasculogenic mimicry related signature predicts the prognosis and immunotherapy response in renal clear cell carcinoma.BMC cancer · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Vasculogenic mimicry (VM), a new model of angiogenesis, fulfills the metabolic demands of solid tumors and contributes to tumor aggressiveness. Our previous study demonstrated the effect of SOX2 in promoting VM in colorectal cancer (CRC). However, the underlying mechanisms behind this effect remain elusive. Here, we show that SOX2 overexpression enhanced glycolysis and sustained VM formation via the transcriptional activation of lncRNA AC005392.2. Suppression of either glycolysis or AC005392.2 expression curbed SOX2-driven VM formation in vivo and in vitro. Mechanistically, SOX2 combined with the promoter of AC005392.2, which decreased H3K27me3 enrichment and thus increased its transcriptional activity. Overexpression of AC005392.2 increased the stability of GLUT1 protein by enhancing its SUMOylation, leading to a decrease in the ubiquitination and degradation of GLUT1. Accumulation of GLUT1 contributed to SOX2-mediated glycolysis and VM. Additionally, clinical analyses showed that increased levels of AC005392.2, GLUT1, and EPHA2 expression were positively correlated with SOX2 and were also associated with poor prognoses in patients with CRC. Our study conclusively demonstrates that the SOX2-lncRNA AC005392.2-GLUT1 signaling axis regulates VM formation in CRC, offering a foundation for the development of new antiangiogenic drugs or new drug combination regimens.
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