ArticleCommunications biology2022
Identifying metabolic reprogramming phenotypes with glycolysis-lipid metabolism discoordination and intercellular communication for lung adenocarcinoma metastasis.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 33 citations in OpenAlex.
- Metabolic pathway signatures define prognostic subtypes of lung adenocarcinoma.Discover oncology · 2026Article
- Establishing a glycolysis-linked multigene prognostic signature in lung adenocarcinoma: a multicenter integrative approach.Journal of thoracic disease · 2025Article
- Peptide Drug: Design and Clinical Applications.MedComm · 2025Review
- The Emerging Roles of Metabolic Reprogramming in Non-Small Cell Lung Cancer Progression.Frontiers in bioscience (Landmark edition) · 2025Review
- Decoding the NRF2-NOTCH Crosstalk in Lung Cancer-An Update.Antioxidants (Basel, Switzerland) · 2025Review
- Dissecting tumor cell programs through group biology estimation in clinical single-cell transcriptomics.Nature communications · 2025Article
- Neurogenic locus notch homolog protein 1 (NOTCH 1) SNP informatics coupled with intrinsically disordered regions and post-translational modifications reveals the complex structural crosstalk of Lung Adenocarcinoma (LUAD).Frontiers in bioinformatics · 2025Article
- Article
- Enigmatic exosomal connection in lung cancer drug resistance.Molecular therapy. Nucleic acids · 2024Review
- Synthetic PET from CT improves diagnosis and prognosis for lung cancer: Proof of concept.Cell reports. Medicine · 2024Article
- High RRM2 Correlates with Mitochondrial and Immune Responses in the Eosinophilic Subtype of Clear Cell Renal Cell Carcinoma.Journal of inflammation research · 2024Article
- SETD2 deficiency accelerates sphingomyelin accumulation and promotes the development of renal cancer.Nature communications · 2023Article
- Identification of distinct tumor cell patterns with single-cell RNA sequencing integrating primary lung adenocarcinoma and brain metastasis tumor.Translational lung cancer research · 2023Article
- Transcriptome data analysis of primary cardiomyopathies reveals perturbations in arachidonic acid metabolism.Frontiers in cardiovascular medicine · 2023Article
- Deep neural network for discovering metabolism-related biomarkers for lung adenocarcinoma.Frontiers in endocrinology · 2023Article
- Comprehensive analysis of the significance of METTL7A gene in the prognosis of lung adenocarcinoma.Frontiers in oncology · 2022Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor metastasis imposes metabolic requirements for escaping from primary tissues, producing vulnerability in treatment. This study aimed to explore the metabolic reprogramming relevant to lung adenocarcinoma (LUAD) metastasis and decode the underlying intercellular alterations. Using the gene expression profiles of 394 LUAD samples derived from The Cancer Genome Atlas (TCGA), we identified 11 metastasis-related metabolic genes involved in glycolysis and lipid metabolism, and defined three metabolic reprogramming phenotypes (MP-I, -II, and -III) using unsupervised clustering. MP-III with the highest glycolytic and lowest lipid metabolic levels exhibited the highest metastatic potency and poorest survival in TCGA and six independent cohorts totaling 1,235 samples. Genomic analyses showed that mutations in TP53 and KEAP1, and deletions in SETD2 and PBRM1 might drive metabolic reprogramming in MP-III. Single-cell RNA-sequencing data from LUAD validated a metabolic evolutionary trajectory from normal to MP-II and MP-III, through MP-I. The further intercellular communications revealed that MP-III interacted uniquely with endothelial cells and fibroblasts in the ANGPTL pathway, and had stronger interactions with endothelial cells in the VEGF pathway. Herein, glycolysis-lipid dysregulation patterns suggested metabolic reprogramming phenotypes relevant to metastasis. Further insights into the oncogenic drivers and microenvironmental interactions would facilitate the treatment of LUAD metastasis in the future.
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