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| http://dx.doi.org/10.1111/all.15253 | DOI Listing |
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Publisher Correction: Starvation-induced metabolic rewiring affects mTORC1 composition in vivo.
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Institute for Biochemistry and Molecular Biology, Medical Faculty, Rheinische Friedrich-Wilhelms-University of Bonn, 53115, Bonn, Germany.
Redirecting glucose flux during in vitro expansion generates epigenetically and metabolically superior T cells for cancer immunotherapy.
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January 2025
Department of Immunology, University of Pittsburgh, Pittsburgh, PA, USA; Tumor Microenvironment Center, UPMC Hillman Cancer Center, Pittsburgh, PA, USA; Department of Pharmacology and Chemical Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address:
Cellular therapies are living drugs whose efficacy depends on persistence and survival. Expansion of therapeutic T cells employs hypermetabolic culture conditions to promote T cell expansion. We show that typical in vitro expansion conditions generate metabolically and functionally impaired T cells more reliant on aerobic glycolysis than those expanding in vivo.
View Article and Find Full Text PDFSelf-healable and pH-responsive spermidine/ferrous ion complexed hydrogel Co-loaded with CA inhibitor and glucose oxidase for combined cancer immunotherapy through triple ferroptosis mechanism.
Bioact Mater
May 2025
Bioscience and Biomedical Engineering Thrust, The Hong Kong University of Science and Technology (Guangzhou), Guangzhou, 511400, China.
Tumor microenvironment governs various therapeutic tolerability of cancer such as ferroptosis and immunotherapy through rewiring tumor metabolic reprogramming like Warburg metabolism. Highly expressed carbonic anhydrases (CA) in tumor that maintaining the delicate metabolic homeostasis is thus the most potential target to be modulated to resolve the therapeutic tolerability. Hence, in this article, a self-healable and pH-responsive spermidine/ferrous ion hydrogel loaded with CA inhibitor (acetazolamide, ACZ) and glucose oxidase (ACZ/GOx@SPM-HA Gel) was fabricated through the Schiff-base reaction between spermidine-dextran and oxidized hyaluronic acid, along with ferrous coordination.
View Article and Find Full Text PDFLINC01224 promotes the Warburg effect in gastric cancer by activating the miR-486-5p/PI3K axis.
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Gastroenterology Section, Medical Center of Digestive Disease, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou, China.
The Warburg effect, a common feature of solid tumors, rewires the metabolism and promotes growth, survival, proliferation, and long-term maintenance in gastric cancer (GC). We performed in vitro and in vivo studies of the pathogenesis of GC to investigate the effects and mechanism of LINC01224 in this cancer. qRT-PCR was used to measure the expression of LINC01224 or miR-486-5p in GC cells, and the expression of LINC01224 in GC tissues by FISH (Fluorescence in situ hybridization) analysis was evaluated.
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Nat Commun
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Institute for Advanced Biosciences, Team: Epigenetics, Immunity, Metabolism, Cell Signaling & Cancer, Inserm U 1209, CNRS UMR 5309, Univ. Grenoble Alpes, Grenoble, France.
Dendritic cells (DC) are key players in antitumor immune responses. Tumors exploit their plasticity to escape immune control; their aberrant surface carbohydrate patterns (e.g.
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