ArticleCell death & disease2025
Platelet-derived exosomal LINC00183 facilitate colorectal cancer malignant progression driven by histone lactylation through stabilizing ENO1.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The research landscape and evolutionary trends of platelet-derived extracellular vesicles: a bibliometric and LDA analysis (2015-2026).Frontiers in oncology · 2026Pooled it
- Lactylation modification in extracellular vesicles: A key regulator of cellular communication.iScience · 2026Review
- Neuron-tumor interplay in colorectal cancer: from mechanisms of onset and progression to targeted therapies.Cell communication and signaling : CCS · 2026Review
- ENO1 as a Central Regulator Linking Metabolic Reprogramming to Tumor Plasticity.International journal of molecular sciences · 2026Review
- Lactylation in Colorectal Cancer: Regulatory Networks, Functional Mechanisms, and Clinical Translational Potential.International journal of molecular sciences · 2026Review
- Extracellular Vesicles as Immunotherapeutic Mediators in Gastrointestinal Cancers and Diseases: From Mechanisms to Clinical Translation.Clinical pharmacology and therapeutics · 2026Review
- Non-coding RNAs in tumor-educated platelets: emerging roles in cancer progression, biomarker discovery, and therapeutic targeting.Frontiers in oncology · 2026Review
- When metabolic enzymes meet lactylation: a bidirectional dialogue in health and disease.Frontiers in cell and developmental biology · 2026Review
- A multidimensional landscape of extracellular vesicle-mediated tumor drug resistance: mechanisms, biomarkers, engineered drug delivery, and clinical translation.Extracellular vesicles and circulating nucleic acids · 2026Review
- Exosome-Mediated Regulation of Aerobic Glycolysis in Hepatocellular Carcinoma: Mechanisms and Therapeutic Implications.Journal of hepatocellular carcinoma · 2026Review
- Exploring exosomal lncRNAs: unlocking the molecular code of tumor metastasis and drug resistance.Cancer cell international · 2025Review
- Targeting Lactylation for Cancer: Mechanisms, Effects, and Therapeutic Prospects.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Platelets play a critical role in tumor progression across various cancers. However, little is known about the molecular mechanisms and biological roles of exosomal long non-coding RNAs (lncRNAs) produced from platelets in colorectal cancer (CRC). Using RNA sequencing, we identified LINC00183 as the most upregulated lncRNA in platelet-derived exosomes (PLT-Exos) from CRC patients, compared to healthy individuals. Analysis of CRC tissue microarrays and TCGA-CRC patient data indicated that LINC00183 is often overexpressed in CRC, in association with advanced tumor stage and poor survival. Effective transfer of exosomal LINC00183 to human CRC cells was verified by FISH, western blotting, and RT-qPCR analyses. Co-incubation with PLT-Exos from CRC patients and overexpression of LINC00183 stimulated the proliferative and invasive capacities of CRC cells. RNA pull-down and RNA immunoprecipitation assays revealed that LINC00183 interacts with enolase 1 (ENO1). This interaction rescues ENO1 from ubiquitin-proteasome-mediated degradation by masking a critical K262 residue. Co-immunoprecipitation, western blotting, CUT&Tag, and gene knockdown and overexpression assays further revealed that the LINC00183-ENO1 interaction activates glycolysis in CRC cells, leading to lactate accumulation, H3K18 lactylation, and transcriptional upregulation of the oncogene GDF15. These results highlight LINC00183 as a possible therapeutic target for CRC.
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