ArticleOpen life sciences2024
Lactate-induced IGF1R protein lactylation promotes proliferation and metabolic reprogramming of lung cancer cells.
Article in Open life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- An externally validated lactylation-associated prognostic signature for overall survival prediction in lung adenocarcinoma identifiesTranslational cancer research · 2026Article
- Role and clinical importance of lactylation in tumors (Review).Molecular medicine reports · 2026Review
- Lactic acid promotes metastasis of papillary thyroid carcinoma by enhancing CPT1A lactylation.Cell death & disease · 2026Article
- Beyond the membrane: Internalization and compartmentalization of insulin‑like growth factor 1 receptor signaling in cancer pathogenesis and treatment (Review).International journal of oncology · 2026Review
- Post-translational protein lactylation modification in lung cancer: an emerging targeted therapeutic strategy.Frontiers in immunology · 2026Review
- Impact of lactylation on the pathogenesis of cancer and its clinical application potential (Review).Molecular medicine reports · 2025Review
- Targeting Lactylation for Cancer: Mechanisms, Effects, and Therapeutic Prospects.International journal of molecular sciences · 2025Review
- Lactylation modification in lung cancer: A review of current research and future directions (Review).Oncology reports · 2025Review
- Research advances of lactylation modification in breast cancer.Discover oncology · 2025Review
- The highly expressedJournal of gastrointestinal oncology · 2025Article
- Lactate metabolism and lactylation in breast cancer: mechanisms and implications.Cancer metastasis reviews · 2025Review
- Lactylation modification in cancer: mechanisms, functions, and therapeutic strategies.Experimental hematology & oncology · 2025Review
- Lactylation in tumor: mechanisms and therapeutic potentials.Frontiers in immunology · 2025Review
- Exploring lactylation and cancer biology: insights from pathogenesis to clinical applications.Frontiers in cell and developmental biology · 2025Review
- Lactylation: a novel driver of drug resistance in the tumor microenvironment.Cancer drug resistance (Alhambra, Calif.) · 2025Review
- A novel lactylation-related gene signature to predict prognosis and treatment response in lung adenocarcinoma.Frontiers in oncology · 2025Article
- Lactylation in health and disease: physiological or pathological?Theranostics · 2025Review
- Potential role of lactylation in intrinsic immune pathways in lung cancer.Frontiers in pharmacology · 2025Review
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Lung cancer (LC) is regarded as a fatal cancer, and insulin-like growth factor 1 (IGF1) and its receptor (IGF1R) have been found to play a key role in regulating tumor glycolytic metabolism. The aim of this study is to investigate LC proliferation regulated by metabolite-mediated IGF1R lactylation. IGF1R was highly expressed in LC tissues and cells, and the effects of IGF1R on protein stability were inhibited by Lactate dehydrogenase A (LDHA) inhibition. Moreover, the tightness of IGF1R binding to IGF1 was also enhanced by exogenous lactic acid but suppressed by LDHA silencing, while cell viability and proliferation were promoted by over-expression of IGF1R. Exogenous lactic acid further exacerbated the effects of the IGF1R gene, while LDHA knocking down reduced the IGF1R-induced malignant behaviors. The IGF1R and exogenous lactic acid were also found to increase extracellular acidification rate (ECAR) and decrease oxygen consumption rate to regulate glycolysis, which was inhibited by LDHA deficiency in LC cells. The study concluded that IGF1R-mediated aggressive behaviors of LC cells were associated with higher levels of IGF1R lactylation. Moreover, lactic acid can improve the protein stability of the IGF1R oncogene, thus promoting glycolysis and generating lactic acid, forming a closed loop. Therefore, targeting IGF1R is envisaged to provide a novel strategy for developing therapeutic agents against LC.
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