ArticleScientific reports2017
Inactivation of HMGCL promotes proliferation and metastasis of nasopharyngeal carcinoma by suppressing oxidative stress.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
- ZNF460 inhibits HMGCL and promotes PI3K pathway in colon cancer.Translational cancer research · 2026Article
- ILF3 Regulates Cell Proliferation and Metastasis by Competitively Antagonizing the Interaction Between HMGCL and USP38 in Hepatocellular Carcinoma.Human mutation · 2026Article
- Identification of potential biomarkers associated with mitochondrial oxidative stress in idiopathic pulmonary arterial hypertension via bioinformatic and experimental analysis.Scientific reports · 2025Article
- HMGCL activates autophagy in osteosarcoma through β-HB mediated inhibition of the PI3K/AKT/mTOR signaling pathway.Journal of translational medicine · 2025Article
- Comprehensive Overview of Ketone Bodies in Cancer Metabolism: Mechanisms and Application.Biomedicines · 2025Review
- Inactivation of Acetyl-CoA Acyltransferase 1 enhances the proliferation and motility of nasopharyngeal carcinoma cells.Molecular & cellular oncology · 2025Article
- Fatty acid metabolism: A new target for nasopharyngeal carcinoma therapy.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024Article
- miR-1202 regulates BPH-1 cell proliferation, apoptosis, and epithelial-to-mesenchymal transition through targeting HMGCL.Acta biochimica et biophysica Sinica · 2024Article
- Metabolic Contrasts: Fatty Acid Oxidation and Ketone Bodies in Healthy Brains vs. Glioblastoma Multiforme.International journal of molecular sciences · 2024Review
- First report on in-depth genome and comparative genome analysis of a metal-resistant bacteriumFrontiers in microbiology · 2024Article
- HMGCL-induced β-hydroxybutyrate production attenuates hepatocellular carcinoma via DPP4-mediated ferroptosis susceptibility.Hepatology international · 2023Article
- Article
- Phosphorylation by IKKβ Promotes the Degradation of HMGCL via NEDD4 in Lung Cancer.International journal of biological sciences · 2023Article
- Molecular Mechanisms for Ketone Body Metabolism, Signaling Functions, and Therapeutic Potential in Cancer.Nutrients · 2022Review
- The Association of Ketolytic Enzymes Gene Expression Levels with Mitochondrial Activity and Content in Oral Squamous Cell CarcinomaAsian Pacific journal of cancer prevention : APJCP · 2022Article
- Ketogenic HMG-CoA lyase and its product β-hydroxybutyrate promote pancreatic cancer progression.The EMBO journal · 2022Article
- EPHX2 Inhibits Colon Cancer Progression by Promoting Fatty Acid Degradation.Frontiers in oncology · 2022Article
- Identification of a VHL gene mutation in atypical Von Hippel-Lindau syndrome: genotype-phenotype correlation and gene therapy perspective.Cancer cell international · 2021Article
- The Aneugenicity of Ketone Bodies in Colon Epithelial Cells Is Mediated by Microtubule Hyperacetylation and Is Blocked by Resveratrol.International journal of molecular sciences · 2021Article
- SDHB Suppresses the Tumorigenesis and Development of ccRCC by Inhibiting Glycolysis.Frontiers in oncology · 2021Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Altered metabolism is considered as a hallmark of cancer. Here we investigated expression of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) 2 lyase (HMGCL), an essential enzyme in ketogenesis, which produces ketone bodies by the breakdown of fatty acids to supply energy, in nasopharyngeal carcinoma (NPC). The expression of HMGCL was silenced in NPC tissue. Downregulation of HMGCL in NPC was associated with low intracellular β-hydroxybutyrate (β-HB) production, thereby reducing reactive oxygen species (ROS) generation. Ectopic expression of HMGCL restored β-HB level, associated with suppressed proliferation and colony formation of NPC cells in vitro and decreased tumorigenicity in vivo. HMGCL suppressed the migration and invasion of NPC cells in vitro via mesenchymal-epithelial transition. Furthermore, extracellular β-HB supply suppressed the proliferation and migration of NPC cells. Both intra- and extracellular β-HB exerting a suppressive role in NPC depends on ROS generation. Ketogenesis may be impaired in NPC cells due to lack of HMGCL expression, suggesting that it may be a promising target in NPC therapy.
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