ArticleCancer research2020
Glucose-6-Phosphate Dehydrogenase Is Not Essential for K-Ras-Driven Tumor Growth or Metastasis.
Article in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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
32 citing papers in PubMed, 44 citations in OpenAlex.
- Role of Esterase BmeFE4 in Mediating the Alleviating Effects of Resveratrol on NaF-Induced Fluorosis inToxics · 2026Article
- Oxidative pentose phosphate pathway is required for T cell activation and antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Review
- Metformin upregulates circadian gene PER2 to inhibit growth and enhance the sensitivity of glioblastoma cell lines to radiotherapy via SIRT2/G6PD pathway.Frontiers in pharmacology · 2025Article
- Characteristics of glucose-6-phosphate dehydrogenase mutations in newborns with deficiency from 2021 to 2022 in the Heze area of China.Frontiers in immunology · 2025Article
- Glucose-6-phosphate dehydrogenase maintains redox homeostasis and biosynthesis in LKB1-deficient KRAS-driven lung cancer.Nature communications · 2024Article
- Regulation of antioxidants in cancer.Molecular cell · 2024Review
- The Role of Tumor Metabolic Reprogramming in Tumor Immunity.International journal of molecular sciences · 2023Review
- Anticancer Peptides Derived from Aldolase A and Induced Tumor-Suppressing Cells Inhibit Pancreatic Ductal Adenocarcinoma Cells.Pharmaceutics · 2023Article
- G6PD Maintains Redox Homeostasis and Biosynthesis in LKB1-Deficient KRAS-Driven Lung Cancer.bioRxiv : the preprint server for biology · 2023Article
- The pentose phosphate pathway in health and disease.Nature metabolism · 2023Review
- Pancreatic cancer epigenetics: adaptive metabolism reprograms starving primary tumors for widespread metastatic outgrowth.Cancer metastasis reviews · 2023Review
- The Role of Reprogrammed Glucose Metabolism in Cancer.Metabolites · 2023Review
- Metabolic reprogramming in colorectal cancer: regulatory networks and therapy.Cell & bioscience · 2023Review
- G6PD-mediated increase in de novo NADPScience advances · 2022Article
- The role of ROS in tumour development and progression.Nature reviews. Cancer · 2022Review
- H3K9me3 represses G6PD expression to suppress the pentose phosphate pathway and ROS production to promote human mesothelioma growth.Oncogene · 2022Article
- Loss of glucose 6-phosphate dehydrogenase function increases oxidative stress and glutaminolysis in metastasizing melanoma cells.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- G6PD functions as a metabolic checkpoint to regulate granzyme B expression in tumor-specific cytotoxic T lymphocytes.Journal for immunotherapy of cancer · 2022Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The enzyme glucose-6-phosphate dehydrogenase (G6PD) is a major contributor to NADPH production and redox homeostasis and its expression is upregulated and correlated with negative patient outcomes in multiple human cancer types. Despite these associations, whether G6PD is essential for tumor initiation, growth, or metastasis remains unclear. Here, we employ modern genetic tools to evaluate the role of G6PD in lung, breast, and colon cancer driven by oncogenic K-Ras. Human HCT116 colorectal cancer cells lacking G6PD exhibited metabolic indicators of oxidative stress, but developed into subcutaneous xenografts with growth comparable with that of wild-type controls. In a genetically engineered mouse model of non-small cell lung cancer driven by K-Ras G12D and p53 deficiency, G6PD knockout did not block formation or proliferation of primary lung tumors. In MDA-MB-231-derived human triple-negative breast cancer cells implanted as orthotopic xenografts, loss of G6PD modestly decreased primary site growth without ablating spontaneous metastasis to the lung and moderately impaired the ability of breast cancer cells to colonize the lung when delivered via tail vein injection. Thus, in the studied K-Ras tumor models, G6PD was not strictly essential for tumorigenesis and at most modestly promoted disease progression. SIGNIFICANCE: K-Ras-driven tumors can grow and metastasize even in the absence of the oxidative pentose pathway, a main NADPH production route.
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Registered trials
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