ArticleOncogene2011
Inhibition of c-Met downregulates TIGAR expression and reduces NADPH production leading to cell death.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- The Impact of TP53-Induced Glycolysis and Apoptosis Regulator on Prognosis in Hepatocellular Carcinoma: Association with Tumor Microenvironment and Ferroptosis.Liver cancer · 2025Article
- Xanthohumol overcomes osimertinib resistance via governing ubiquitination-modulated Ets-1 turnover.Cell death discovery · 2024Article
- E2F1-Associated Purine Synthesis Pathway Is a Major Component of the MET-DNA Damage Response Network.Cancer research communications · 2024Article
- Article
- Reduced nicotinamide adenine dinucleotide phosphate in redox balance and diseases: a friend or foe?Acta pharmacologica Sinica · 2022Review
- The role of ROS in tumour development and progression.Nature reviews. Cancer · 2022Review
- Structure, regulation, and biological functions of TIGAR and its role in diseases.Acta pharmacologica Sinica · 2021Review
- In silico identification of potential inhibitor for TP53-induced glycolysis and apoptosis regulator in head and neck squamous cell carcinoma.3 Biotech · 2021Article
- LncRNA MACC1-AS1/MACC1 enhances the progression of glioma via regulating metabolic plasticity.Cell cycle (Georgetown, Tex.) · 2020Article
- Metabolic remodeling by TIGAR overexpression is a therapeutic target in esophageal squamous-cell carcinoma.Theranostics · 2020Article
- Genome-scale CRISPR knockout screen identifiesCommunications biology · 2019Article
- Cancer-Associated Fibroblasts Drive Glycolysis in a Targetable Signaling Loop Implicated in Head and Neck Squamous Cell Carcinoma Progression.Cancer research · 2018Article
- The fructose-2,6-bisphosphatase TIGAR suppresses NF-κB signaling by directly inhibiting the linear ubiquitin assembly complex LUBAC.The Journal of biological chemistry · 2018Article
- Met is involved in TIGAR-regulated metastasis of non-small-cell lung cancer.Molecular cancer · 2018Article
- The lncRNA MACC1-AS1 promotes gastric cancer cell metabolic plasticity via AMPK/Lin28 mediated mRNA stability of MACC1.Molecular cancer · 2018Article
- The relevance of tyrosine kinase inhibitors for global metabolic pathways in cancer.Molecular cancer · 2018Review
- Cancer metabolism: New insights into classic characteristics.The Japanese dental science review · 2018Review
- Fructose 2,6-Bisphosphate in Cancer Cell Metabolism.Frontiers in oncology · 2018Review
- ROS in Cancer: The Burning Question.Trends in molecular medicine · 2017Review
- Hepatocyte Growth Factor/c-Met Signaling in Head and Neck Cancer and Implications for Treatment.Cancers · 2017Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
Abstract
c-Met represents an important emerging therapeutic target in cancer. In this study, we demonstrate the mechanism by which c-Met tyrosine kinase inhibition inhibits tumor growth in a highly invasive Asian-prevalent head and neck cancer, nasopharyngeal cancer (NPC). c-Met tyrosine kinase inhibitors (TKIs; AM7 and c-Met TKI tool compound SU11274) downregulated c-Met phosphorylation, resulting in marked inhibition of NPC cell growth and invasion. Strikingly, inhibition of c-Met resulted in significant downregulation of TP53-induced Glycolysis and Apoptosis Regulator (TIGAR) and subsequent depletion of intracellular NADPH. Importantly, overexpression of TIGAR ameliorated the effects of c-Met kinase inhibition, confirming the importance of TIGAR downregulation in the growth inhibitory activity of c-Met TKI. The effects of c-Met inhibition on TIGAR and NADPH levels were observed with two different c-Met TKIs (AM7 and SU11274) and with multiple cell lines. As NADPH provides a crucial reducing power required for cell survival and proliferation, our findings reveal a novel mechanistic action of c-Met TKI, which may represent a key effect of c-Met kinase inhibition. Our data provide the first evidence linking c-Met, TIGAR and NADPH regulation in human cancer cells suggesting that inhibition of a tyrosine kinase/TIGAR/NADPH cascade may have therapeutic applicability in human cancers.
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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.