ArticleCommunications biology2025
CPT2 inhibition enhances selective autophagy and proliferation in colorectal cancer via GPAT4-dependent glycerophospholipid biosynthesis.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- GPAT4 regulates antitumor immune response through activating the mtDNA-cGAS axis in cancer cells.Cell insight · 2026Article
- Development and verification of a lipotoxicity-related gene signature for predicting prognosis and immune landscape in colorectal cancer.Discover oncology · 2026Article
- CDK13 drives clear cell renal carcinoma through METTL16-mediated mExperimental & molecular medicine · 2026Article
- Microbial metabolic profiling reshapes NF-κB-mediated immune metabolic network: a new mechanism for CRC development.Journal of translational medicine · 2026Review
- Organelle-specific regulation of ferroptosis.Biology direct · 2026Review
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Authors and funding
15 authors.
Funding
Abstract
Metabolic reprogramming is one of the hallmark events in colorectal cancer. Tumor cells adapt to microenvironmental changes by regulating energy and biomaterial metabolism. This study identifys abnormal lipid accumulation and significant downregulation of fatty acid metabolism in colorectal cancer. The core gene of this pathway, CPT2, critically impacts colorectal cancer patient survival and regulates tumor cell proliferation both in vitro and in vivo. Metabolite analysis demonstrates that CPT2 knockdown induced accumulation of glycerophospholipids, primarily phosphatidylcholine and phosphatidylethanolamine, driven by enhanced long-chain fatty acid-dependent glycerophospholipid biosynthesis mediated by GPAT4. Transcriptomic analysis and subsequent experiments reveal that glycerophospholipid accumulation, as key components of vesicles and autophagosomes, promoted autophagosome maturation and elongation, thereby activating selective autophagy (lipophagy) in colorectal cancer cells and accelerating tumor progression. These findings enhance understanding of tumor metabolic characteristics and identify novel diagnostic and therapeutic targets for colorectal cancer.
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