ArticleCancer gene therapy2023
M2 macrophage exosomal LINC01001 promotes non-small cell lung cancer development by affecting METTL3 and glycolysis pathway.
Article in Cancer gene therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 5 citations in OpenAlex.
- M2 macrophage-derived exosomal EHF transcriptionally activates FGFR1 to promote malignant phenotypes and glycolysis in NSCLC.Journal of bioenergetics and biomembranes · 2026Article
- Macrophages in lung cancer: principal factors, regulatory mechanisms, and therapeutic opportunities: a narrative review.Translational lung cancer research · 2026Review
- Nanomedicine novel strategies: deciphering the EV-metabolic axis as a natural nanocarrier network in lung cancer progression and cachexia.Journal of nanobiotechnology · 2026Review
- Macrophage-derived long non-coding RNAs in cancer: pioneering targets for immune modulation and personalized therapy.Frontiers in immunology · 2026Review
- The inhibitory effect of M2 macrophage-derived exosomes on gefitinib resistant lung adenocarcinoma cells through the MIF/TIMP1/CD74 axis.Scientific reports · 2025Article
- A novel classification method for LUAD that guides personalized immunotherapy on the basis of the cross-talk of coagulation- and macrophage-related genes.Frontiers in immunology · 2025Article
- Association between methyltransferase-like 3 and non-small cell lung cancer: pathogenesis, therapeutic resistance, and clinical applications.Translational lung cancer research · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
There have been data showing that LINC01001 is highly expressed in lung cancer, but the effect of M2 macrophage exosomal LINC01001 to METTL3, glycolysis and immunity in non-small cell lung cancer (NSCLC) has not been reported. In this study, we aimed to explore the regulatory effect and mechanism of M2 macrophage exosomal LINC01001 in NSCLC. The results of our study show that the verification of macrophage exosomes, it was confirmed that exosomes regulated proliferation, glucose intake, lactate production and ATP levels of NSCLC cells. Exosomes also promoted the expression of METTL3. Bioinformatics screening showed that LINC01001 regulated METTL3. Subsequent experiments revealed exosomal LINC01001 influenced the glycolysis processes of NSCLC cells. Through RIP, it was proved that LINC01001 functioned in combination with METTL3. Bioinformatics predicted that NASP was a METTL3-targeted gene. LINC01001 could also regulate NASP methylation. Tumorigenesis in mice also indicated that LINC01001 mediated METTL3 to stimulate the development of tumors. In this study, LINC01001 was successfully verified in the exosomes-derived from M2 macrophages. It was confirmed that LINC01001 could interact with METTL3 and regulate glycolysis process in NSCLC cells. LINC01001 also inhibited T cell proliferation.
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Registered trials
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