ArticleOncogene2020
Cancer progression is mediated by proline catabolism in non-small cell lung cancer.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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Who cites it
51 citing papers in PubMed, 76 citations in OpenAlex.
- Identification of a candidate PRODH allosteric inhibitor MBTP-15324: modulation of proline metabolite profiles and ECM-associated gene-expression changes in lung cancer cells.Journal of enzyme inhibition and medicinal chemistry · 2026Article
- SEFA: Semantic Embedding-Based Feature Augmentation of Biomedical Language-Model Embeddings Improves Interpretable Metabolomic Prediction of Lung Cancer.Biomedicines · 2026Article
- AHSA1 promotes the progression of lung cancer by enhancing the expression of HSP90α.Histology and histopathology · 2026Article
- Proline Metabolism in Cancer: Emerging Roles in Redox Homeostasis and Therapeutic Opportunities.Cancers · 2025Review
- Amino acids shape the metabolic and immunologic landscape in the tumor immune microenvironment: from molecular mechanisms to therapeutic strategies.Cancer biology & medicine · 2025Review
- Amino acids in cancer: Understanding metabolic plasticity and divergence for better therapeutic approaches.Cell reports · 2025Review
- Taurine and proline promote lung tumour growth by co-regulating Azgp1/mTOR signalling pathway.NPJ precision oncology · 2025Article
- Metabolic reprogramming and therapeutic targeting in non-small cell lung cancer: emerging insights beyond the Warburg effect.Frontiers in oncology · 2025Review
- Deciphering molecular pathways driving cancer invasion and metastasis: advances and therapeutic prospects.Frontiers in oncology · 2025Review
- Article
- The bioenergetic landscape of cancer.Molecular metabolism · 2024Review
- Deciphering glutamine metabolism patterns for malignancy and tumor microenvironment in clear cell renal cell carcinoma.Clinical and experimental medicine · 2024Article
- PPP2R1A silencing suppresses LUAD progression by sensitizing cells to nelfinavir-induced apoptosis and pyroptosis.Cancer cell international · 2024Article
- Proline Dehydrogenase (PRODH) Is Expressed in Lung Adenocarcinoma and Modulates Cell Survival and 3D Growth by Inducing Cellular Senescence.International journal of molecular sciences · 2024Article
- The Role of Amino Acids in Non-Enzymatic Antioxidant Mechanisms in Cancer: A Review.Metabolites · 2023Review
- LINC02774 inhibits glycolysis in glioma to destabilize HIF-1α dependent on transcription factor RP58.MedComm · 2023Article
- Loss of attachment promotes proline accumulation and excretion in cancer cells.Science advances · 2023Article
- Identification of age- and immune-related gene signatures for clinical outcome prediction in lung adenocarcinoma.Cancer medicine · 2023Article
- Dietary Manipulation of Amino Acids for Cancer Therapy.Nutrients · 2023Review
- Plasticity of cancer invasion and energy metabolism.Trends in cell biology · 2023Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulated metabolism contributes to cancer initiation and progression, but the key drivers of these pathways are just being discovered. Here, we report a critical role for proline catabolism in non-small cell lung cancer (NSCLC). Proline dehydrogenase (PRODH) is activated to reduce proline levels by the chromatin remodeling factor lymphoid-specific helicase (LSH), an epigenetic driver of NSCLC. PRODH promotes NSCLC tumorigenesis by inducing epithelial to mesenchymal transition (EMT) and IKKα-dependent inflammatory genes, including CXCL1, LCN2, and IL17C. Consistently, proline addition promotes the expression of these inflammatory genes, as well as EMT, tumor cell proliferation, and migration in vitro and tumor growth in vivo, while the depletion or inhibition of PRODH blocks these phenotypes. In summary, we reveal an essential metabolic pathway amenable to targeting in NSCLC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.