ArticleBMC cancer2018
Inhibition of glutamate oxaloacetate transaminase 1 in cancer cell lines results in altered metabolism with increased dependency of glucose.
Article in BMC cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 87 citations in OpenAlex.
- Why is the tumor microenvironment disordered by NADH/NADRedox biology · 2026Review
- Mechanisms Underlying Drought Adaptability in Duolang Sheep Based on Metabolomic and Transcriptomic Analyses.Biology · 2026Article
- Exploring the correlation between ferroptosis-associated biomarkers and MRI-derived parameters in liver fibrosis associated with metabolic dysfunction-associated steatotic liver disease.Clinical and experimental medicine · 2026Article
- WSSV-induced reversal of the malate-aspartate shuttle facilitates viral replication in shrimp hemocytes.Cell communication and signaling : CCS · 2025Article
- Exploring the multifaceted roles of glutamate oxaloacetate transaminase 1 as a biomarker and therapeutic target in colorectal cancer and pan-cancer analyses.Discover oncology · 2025Article
- Mitochondrial metabolic reprogramming in colorectal cancer: mechanisms of resistance and future clinical interventions.Cell death discovery · 2025Review
- SIRT1 maintains bone homeostasis by regulating osteoblast glycolysis through GOT1.Cellular and molecular life sciences : CMLS · 2024Article
- Review
- Identification of candidate regulatory genes for intramuscular fatty acid composition in pigs by transcriptome analysis.Genetics, selection, evolution : GSE · 2024Article
- The Tricarboxylic Acid Cycle Metabolites for Cancer: Friend or Enemy.Research (Washington, D.C.) · 2024Review
- The role of GOT1 in cancer metabolism.Frontiers in oncology · 2024Review
- Advances in Drug Therapy for Metastatic Pancreatic Ductal Adenocarcinoma.Journal of Cancer · 2024Review
- Review
- Mitochondrial phosphoenolpyruvate carboxykinase inhibits kidney renal clear cell carcinoma malignant progression, leading to cell energy metabolism imbalance.American journal of cancer research · 2023Article
- Applications and advancements of CRISPR-Cas in the treatment of lung cancer.Frontiers in cell and developmental biology · 2023Review
- An Overview: The Diversified Role of Mitochondria in Cancer Metabolism.International journal of biological sciences · 2023Review
- Transcriptome Analysis of Goat Mammary Gland Tissue Reveals the Adaptive Strategies and Molecular Mechanisms of Lactation and Involution.International journal of molecular sciences · 2022Article
- Assessment of a Large-Scale Unbiased Malignant Pleural Effusion Proteomics Study of a Real-Life Cohort.Cancers · 2022Article
- Osteoblasts induce glucose-derived ATP perturbations in chondrocytes through noncontact communication.Acta biochimica et biophysica Sinica · 2022Article
- Ziprasidone suppresses pancreatic adenocarcinoma cell proliferation by targeting GOT1 to trigger glutamine metabolism reprogramming.Journal of molecular medicine (Berlin, Germany) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundGlutamate oxaloacetate transaminase 1 (GOT1) regulates cellular metabolism through coordinating the utilization of carbohydrates and amino acids to meet nutrient requirements. KRAS mutated cancer cells were recently shown to rely on GOT1 to support long-term cell proliferation. The aim of the present study was to address the role of GOT1 in the metabolic adaption of cancer cells.
methodsGOT1-null and knockdown cell lines were established through CRISPR/Cas9 and shRNA techniques. The growth properties, colony formation ability, autophagy and selected gene expression profiles were analysed. Glucose deprivation decreased the viability of the GOT1-null cells and rescue experiments were conducted with selected intermediates. The redox NADH/NAD
resultsInhibition of GOT1 sensitized the cancer cells to glucose deprivation, which was partially counteracted by oxaloacetate and phosphoenol pyruvate, metabolic intermediates downstream of GOT1. Moreover, GOT1-null cells accumulated NADH and displayed a decreased ratio of NADH/NAD
conclusionsOur study suggests an important role of GOT1 to coordinate the glycolytic and the oxidative phosphorylation pathways in KRAS mutated cancer cells. GOT1 is crucial to provide oxaloacetate at low glucose levels, likely to maintain the redox homeostasis. Our data suggest GOT1 as a possible target in cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.