ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Targeting Metabolic Adaptation of Colorectal Cancer with Vanadium-Doped Nanosystem to Enhance Chemotherapy and Immunotherapy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Metabolic reprogramming in colorectal cancer: Mechanisms and therapeutic insights.Genes & diseases · 2027Review
- Nanocarrier strategies to overcome P-glycoprotein-mediated drug resistance in cancer therapy.Beilstein journal of nanotechnology · 2026Review
- Diversion ostomy improves treatment tolerance, conversion surgery, and survival compared with self-expanding metal stenting in initially unresectable obstructive colorectal cancer.Frontiers in oncology · 2026Article
- Simple-synthesis VO₂ nanoparticles as robust nanozymes for synergistic antibacterial therapy and abscess repair.Journal of nanobiotechnology · 2025Article
- Mitochondrial metabolic reprogramming in colorectal cancer: mechanisms of resistance and future clinical interventions.Cell death discovery · 2025Review
- Targeting Metabolic Adaptation of Colorectal Cancer with Vanadium-Doped Nanosystem to Enhance Chemotherapy and Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The anti-tumor efficacy of current pharmacotherapy is severely hampered due to the adaptive evolution of tumors, urgently needing effective therapeutic strategies capable of breaking such adaptability. Metabolic reprogramming, as an adaptive survival mechanism, is closely related to therapy resistance of tumors. Colorectal cancer (CRC) cells exhibit a high energy dependency that is sustained by an adaptive metabolic conversion between glucose and glutamine, helping tumor cells to withstand nutrient-deficient microenvironments and various treatments. We discover that transition metal vanadium (V) effectively inhibits glucose metabolism in CRC and synergizes with glutaminase inhibitors (BPTES) to disrupt CRC's energy dependency. Thus, a dual energy metabolism suppression nanosystem (VSi-BP@HA) is engineered by loading BPTES into V-doped hollow mesoporous silica nanoparticles. This nanosystem effectively dampens CRC energy metabolism, eradicating 33% of tumors in mice. Strikingly, the cell biological and preclinical model datasets provide compelling evidence showing that VSi-BP@HA not only reverses CRC cells chemo-resistance but also drastically potentiates anti-PD1 immunotherapy. Therefore, this nanosystem provides not only a promising approach to suppress CRC, but also a potential adjunct tool for enhancing chemotherapy and immunotherapy.
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Registered trials
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.