ReviewFrontiers in cell and developmental biology2025
Targeting Wnt-driven metabolic adaptations in cancer: integrating glycolysis, glutaminolysis, IDO1-mediated immune evasion, and therapeutic delivery strategies.
Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Systems biology of Wnt signaling in glioma chemotherapy resistance: Integrating multi-omics mechanisms and emerging therapeutic vulnerabilities (Review).Oncology letters · 2026Review
- Downregulation of LRRC59 suppresses cervical cancer progression likely by inhibiting YBX1-mediated Wnt/β-catenin signaling.Scientific reports · 2026Article
- Refined Jianpi Huayu Jiedu Decoction Attenuates TAM-Induced Spasmolytic Polypeptide-Expressing Metaplasia (SPEM) by Modulating LCN2-Associated Mitochondrial Dysfunction.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Single-cell capture of on-ART SIV transcription reveals TGF-β-mediated metabolic control of viral latency.JCI insight · 2026Article
- PRMT3 in cancer: arginine methylation as a driver of tumor metabolism, immune evasion, and therapeutic resistance.Frontiers in immunology · 2026Review
- Linking the Warburg effect to endometrial receptivity: metabolic parallels in embryo implantation.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
4 authors.
Funding
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Abstract
The Wnt pathway is an evolutionarily conserved signaling cascade that regulates a wide range of fundamental cellular processes, including proliferation, differentiation, polarity, migration, metabolism, and survival. Due to its central regulatory roles, Wnt signaling is critically involved in the pathophysiology of numerous human diseases. Aberrant activation or insufficient inhibition of this pathway has been causally linked to cancer, degenerative disorders, metabolic syndromes, and developmental abnormalities. Wnt signaling drives cancer progression by reprogramming metabolism and promoting immune evasion. Wnt-driven tumors exhibit enhanced aerobic glycolysis (the Warburg effect), glutaminolysis, and macropinocytosis, which support rapid proliferation and help maintain redox homeostasis under nutrient-limited or nutrient-deprived conditions. These metabolic adaptations sustain tumor survival and contribute to immune suppression, as seen in the Wnt5a-indoleamine 2,3-dioxygenase 1 (IDO1) axis, which fosters regulatory T-cell expansion and an immunosuppressive microenvironment. The interplay among glycolysis, glutamine metabolism, and immune escape renders Wnt-driven cancers highly adaptable and resistant to conventional therapies. Targeting metabolic enzymes, such as pyruvate dehydrogenase kinase 1 (PDK1), lactate dehydrogenase A (LDHA), glutaminase (GLS), and monocarboxylate transporters (MCT-1), alongside immune checkpoint inhibitors or IDO1 blockade, presents a promising strategy for overcoming metabolic plasticity and immune evasion in Wnt-driven malignancies, thereby enhancing therapeutic efficacy and improving patient survival in otherwise refractory tumor types. Combining glycolysis and glutaminolysis inhibitors with T-cell activating therapies may disrupt tumor metabolic plasticity and restore anti-tumor immunity. Additionally, advanced drug delivery systems, including lipid nanoparticles (LNPs), polymeric nanocarriers, and exosome-based platforms, enhance the targeted accumulation of metabolic inhibitors and immunomodulatory agents while minimizing systemic toxicity. This review examines the metabolic and immune adaptations of Wnt-driven cancers, with a focus on glycolysis, glutaminolysis, and macropinocytosis. We highlight emerging therapeutic targets and nanomedicine-based delivery strategies to counteract metabolic adaptation and immune suppression. By integrating metabolic and immune-targeting with precision nano-delivery platforms, future treatment paradigms may improve outcomes for aggressive and therapy-resistant Wnt-driven cancers.
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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 Socratic graph.