ArticleCancer medicine2018
Oxaloacetate induces apoptosis in HepG2 cells via inhibition of glycolysis.
Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Absolute dynamic and relative static: the relationship of glycolysis and OXPHOS in cancer development.Cell death discovery · 2026Review
- ENO1 Knockdown Impedes Tumour Progression and Promotes Oxidative Phosphorylation in Cutaneous Squamous Cell Carcinoma.Acta dermato-venereologica · 2025Article
- Anticancer Activity ofBiomolecules · 2025Article
- Hypoxia signaling in the adipose tissue.Journal of molecular cell biology · 2025Review
- Sodium citrate targeting CaJournal of advanced research · 2024Article
- Oxaloacetate as new inducer for osteogenic differentiation of human adipose tissue-derived mesenchymal stem cells in vitro.Molecular biology reports · 2024Article
- The Tricarboxylic Acid Cycle Metabolites for Cancer: Friend or Enemy.Research (Washington, D.C.) · 2024Review
- Cryptocaryone induces apoptosis in human hepatocellular carcinoma cells by inhibiting aerobic glycolysis through Akt and c-Src signaling pathways.Journal of food and drug analysis · 2023Article
- c-Myc protects hepatocellular carcinoma cell from ferroptosis induced by glutamine deprivation via upregulating GOT1 and Nrf2.Molecular biology reports · 2023Article
- Mitochondrial aconitase suppresses immunity by modulating oxaloacetate and the mitochondrial unfolded protein response.Nature communications · 2023Article
- An Overview: The Diversified Role of Mitochondria in Cancer Metabolism.International journal of biological sciences · 2023Review
- Looking for the Holy Grail-Drug Candidates for Glioblastoma Multiforme Chemotherapy.Biomedicines · 2022Review
- MiR-652-5p elevated glycolysis level by targeting TIGAR in T-cell acute lymphoblastic leukemia.Cell death & disease · 2022Article
- The Metabolic Response of Various Cell Lines to Microtubule-Driven Uptake of Lipid- and Polymer-Coated Layer-by-Layer Microcarriers.Pharmaceutics · 2021Article
- The functional roles of TCA cycle metabolites in cancer.Oncogene · 2021Review
- Serum Metabolomics Study of Papillary Thyroid Carcinoma Based on HPLC-Q-TOF-MS/MS.Frontiers in cell and developmental biology · 2021Article
- Perimitochondrial Enzymatic Self-Assembly for Selective Targeting the Mitochondria of Cancer Cells.ACS nano · 2020Article
- Extracellular Citrate Is a Trojan Horse for Cancer Cells.Frontiers in molecular biosciences · 2020Article
- Immunogenomic Profiling and Classification of Prostate Cancer Based on HIF-1 Signaling Pathway.Frontiers in oncology · 2020Article
- Serum metabolomic alterations in multiple myeloma revealed by targeted and untargeted metabolomics approaches: a pilot study.RSC advances · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Most cancer cells perform glycolysis despite having sufficient oxygen. The specific metabolic pathways of cancer cells have become the focus of cancer treatment. Recently, accumulating evidence indicates oxidative phosphorylation (OXPHOS) and glycolysis can be regulated with each other. Thus, we suggest that the glycolysis of cancer cells is inhibited by restoring or improving OXPHOS in cancer cells. In our study, we found that oxaloacetate (OA) induced apoptosis in HepG2 cells in vivo and in vitro. Meanwhile, we found that OA induced a decrease in the energy metabolism of HepG2 cells. Further results showed that the expression and activity of glycolytic enzymes were decreased with OA treatment. Conversely, the expression and activity of enzymes involved in the TCA cycle and OXPHOS were increased with OA treatment. The results indicate that OA can inhibit glycolysis through enhancement of OXPHOS. In addition, OA-mediated suppression of HIF1α, p-Akt, and c-myc led to a decrease in glycolysis level. Therefore, OA has the potential to be a novel anticancer drug.
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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.