ArticlePloS one2014
Regulation and novel action of thymidine phosphorylase in non-small cell lung cancer: crosstalk with Nrf2 and HO-1.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Oxidative Stress Defense Module in Lung Cancers: Molecular Pathways and Therapeutic Approaches.Antioxidants (Basel, Switzerland) · 2025Review
- The senescence-associated secretome of Hedgehog-deficient hepatocytes drives MASLD progression.The Journal of clinical investigation · 2024Article
- Antioxidant genes in cancer and metabolic diseases: Focusing on Nrf2, Sestrin, and heme oxygenase 1.International journal of biological sciences · 2024Review
- Heme Oxygenase-1 and Its Role in Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- Modulation of Nrf2/HO-1 by Natural Compounds in Lung Cancer.Antioxidants (Basel, Switzerland) · 2023Review
- High Hemin Concentration Induces Escape from Senescence of Normoxic and Hypoxic Colon Cancer Cells.Cancers · 2022Article
- Article
- Review
- Tin Mesoporphyrin Selectively Reduces Non-Small-Cell Lung Cancer Cell Line A549 Proliferation by Interfering with Heme Oxygenase and Glutathione Systems.Biomolecules · 2021Article
- The Diverse Roles of Heme Oxygenase-1 in Tumor Progression.Frontiers in immunology · 2021Review
- Nrf2 Mediates Metabolic Reprogramming in Non-Small Cell Lung Cancer.Frontiers in oncology · 2020Review
- The Roles of NRF2 in Modulating Cellular Iron Homeostasis.Antioxidants & redox signaling · 2018Review
- HO-1 Induction in Cancer Progression: A Matter of Cell Adaptation.Antioxidants (Basel, Switzerland) · 2017Review
- Emerging roles of Nrf2 signal in non-small cell lung cancer.Journal of hematology & oncology · 2016Review
- Induction of heme oxygenase-1 by hemin protects lung against orthotopic autologous liver transplantation-induced acute lung injury in rats.Journal of translational medicine · 2016Article
- The Role of miR-378a in Metabolism, Angiogenesis, and Muscle Biology.International journal of endocrinology · 2015Review
- The antioxidant paradox: what are antioxidants and how should they be used in a therapeutic context for cancer.Future medicinal chemistry · 2014Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Proangiogenic enzyme thymidine phosphorylase (TP) is a promising target for anticancer therapy, yet its action in non-small cell lung carcinoma (NSCLC) is not fully understood. To elucidate its role in NSCLC tumor growth, NCI-H292 lung mucoepidermoid carcinoma cells and endothelial cells were engineered to overexpress TP by viral vector transduction. NSCLC cells with altered expression of transcription factor Nrf2 or its target gene heme oxygenase-1 (HO-1) were used to study the regulation of TP and the findings from pre-clinical models were related to gene expression data from clinical NSCLC specimens. Overexpression of Nrf2 or HO-1 resulted in upregulation of TP in NCI-H292 cells, an effect mimicked by treatment with an antioxidant N-acetylcysteine and partially reversed by HO-1 knockdown. Overexpression of TP attenuated cell proliferation and migration in vitro, but simultaneously enhanced angiogenic potential of cancer cells supplemented with thymidine. The latter was also observed for SK-MES-1 squamous cell carcinoma and NCI-H460 large cell carcinoma cells. TP-overexpressing NCI-H292 tumors in vivo exhibited better oxygenation and higher expression of IL-8, IL-1β and IL-6. TP overexpression in endothelial cells augmented their angiogenic properties which was associated with enhanced generation of HO-1 and VEGF. Correlation of TP with the expression of HO-1 and inflammatory cytokines was confirmed in clinical samples of NSCLC. Altogether, the increased expression of IL-1β and IL-6 together with proangiogenic effects of TP-expressing NSCLC on endothelium can contribute to tumor growth, implying TP as a target for antiangiogenesis 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.