ArticleMolecular cell2017
Paraoxonase 2 Facilitates Pancreatic Cancer Growth and Metastasis by Stimulating GLUT1-Mediated Glucose Transport.
Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Modern Approaches to Diagnosis and Evaluation of Survival Prognosis in Patients with Pancreatic Cancer.International journal of molecular sciences · 2026Pooled it
- The regulatory roles of non-coding RNAs in aerobic glycolysis and therapeutic potential in pancreatic ductal adenocarcinoma.Annals of medicine · 2026Review
- Glucose Transporters: Structure, Trafficking, Physiology, and Disease Relevance.Current issues in molecular biology · 2026Review
- The dual role of AMPK in cancer metabolic reprogramming.Molecular biology reports · 2026Review
- Upregulation of paraoxonase-2 enzyme in human osteosarcoma and its involvement in mechanisms promoting the aggressive behavior of tumor cells.Molecular biology reports · 2026Article
- Paraoxonases as metabolic and signaling modulators: prospects for therapeutic and preventive implications.npj metabolic health and disease · 2026Review
- Granzyme B-based CAR-T cells targeting membrane-bound HSP70 suppress solid tumor growth and metastasis.Oncogene · 2026Article
- GLUT6-facilitated noncanonical glucose metabolic rewiring enables resistance to targeted cancer therapy.Nature communications · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- AMPK-activated BAP1 regulates pVHL stability and tumor-suppressive functions.Cell death and differentiation · 2026Article
- Mutant p53 Regulates Pyruvate Dehydrogenase Kinase 1 (PDK1) to Promote Proliferation and Migration in Breast Cancer.Cancer science · 2026Article
- Sensitising PDAC to Gemcitabine by Suppressing NF-κB Pathway and Enhancing Apoptosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Anoctamin 5 mutation leads to abnormal bone homeostasis of GDD by regulating AMPK-dependent glucose metabolism.Frontiers in endocrinology · 2026Article
- Unraveling the anoikis-cancer nexus: a bibliometric analysis of research trends and mechanisms.Future science OA · 2025Article
- Glutaminase inhibition ameliorates cancer-associated fibroblast lipid support of pancreatic cancer cell growth.Cancer & metabolism · 2025Article
- Role of paraoxonase 2 (PON2) as a potential biomarker and therapeutic target in cancer treatment.Journal of cancer research and clinical oncology · 2025Review
- Paraoxonase 3 regulates the pore-forming α subunit of the large-conductance KBiochimica et biophysica acta. Molecular cell research · 2025Article
- Warburg effect and lactylation in cancer: mechanisms for chemoresistance.Molecular medicine (Cambridge, Mass.) · 2025Review
- Transcriptional regulation and post-translational modifications in the glycolytic pathway for targeted cancer therapy.Acta pharmacologica Sinica · 2024Review
- Antiapoptotic PON2 expression and its clinical implications in locally advanced oral squamous cell carcinoma.Cancer science · 2024Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Metabolic deregulation is a hallmark of human cancers, and the glycolytic and glutamine metabolism pathways were shown to be deregulated in pancreatic ductal adenocarcinoma (PDAC). To identify new metabolic regulators of PDAC tumor growth and metastasis, we systematically knocked down metabolic genes that were overexpressed in human PDAC tumor samples using short hairpin RNAs. We found that p53 transcriptionally represses paraoxonase 2 (PON2), which regulates GLUT1-mediated glucose transport via stomatin. The loss of PON2 initiates the cellular starvation response and activates AMP-activated protein kinase (AMPK). In turn, AMPK activates FOXO3A and its transcriptional target, PUMA, which induces anoikis to suppress PDAC tumor growth and metastasis. Pharmacological or genetic activation of AMPK, similar to PON2 inhibition, blocks PDAC tumor growth. Collectively, our results identify PON2 as a new modulator of glucose transport that regulates a pharmacologically tractable pathway necessary for PDAC tumor growth and metastasis.
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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.