ArticleActa pharmaceutica Sinica. B2022
Targeting PFKL with penfluridol inhibits glycolysis and suppresses esophageal cancer tumorigenesis in an AMPK/FOXO3a/BIM-dependent manner.
Article in Acta pharmaceutica Sinica. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 86 citations in OpenAlex.
- Unraveling the molecular landscape and therapeutic strategies for acute kidney injury: insights from transcriptomics, network pharmacology, virtual screening, and in vitro experiments.Molecular diversity · 2026Article
- Penfluridol directly targets PDPK1 to suppress AKT1 phosphorylation and stabilize CTR1, inducing cuproptosis in colorectal cancer.Acta pharmacologica Sinica · 2026Article
- Lactylation Modification and Esophageal Cancer: Research Progress From Hypoxia-Induced Metabolic Reprogramming to Immune Escape.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
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- Lactylation modification in extracellular vesicles: A key regulator of cellular communication.iScience · 2026Review
- A Noncanonical RNA-Binding Function of NQO1 Drives Angiogenesis in Esophageal Squamous Cell Carcinoma via Extracellular Vesicle-Mediated AGRN Transfer.Cancer research · 2026Article
- The oral microbiome is associated with the diagnosis, prognosis and radiotherapy sensitivity of esophageal cancer.Journal of translational medicine · 2026Article
- Interacting proteins of AMPK studied using TurboID proximity labeling technology.Experimental and therapeutic medicine · 2026Article
- Esophageal cancer: from pathogenesis to precision therapies.Signal transduction and targeted therapy · 2026Review
- Neuro-tumor interactions in peripheral tumors.Cancer metastasis reviews · 2026Review
- Adh1-Programmed SNF1 Phosphogradients Decrypt Morphogenesis in Candida albicans: Chemical Interrogation Unveils Hyphal Transition Thresholds.Microbial biotechnology · 2026Article
- Fluvastatin suppresses breast cancer initiation and progression via targeting CYP4Z1.Communications biology · 2026Article
- Role and Molecular Mechanisms of Aerobic Glycolysis in Gastrointestinal Tumors.Journal of Cancer · 2026Review
- Biological Performance and Molecular Mechanisms of Mesyl MicroRNA-Targeted Oligonucleotides in Colorectal Cancer Cells.International journal of molecular sciences · 2025Article
- Hypoxia-Induced m6A modification via YTHDF2 stabilizes PFKL to fuel MDSC Glycolysis and hepatocellular carcinoma progression.Functional & integrative genomics · 2025Article
- The noncanonical function of liver-type phosphofructokinase potentiates the efficacy of HDAC inhibitors in cancer.Signal transduction and targeted therapy · 2025Article
- Review
- Phosphofructokinase-1 redefined: a metabolic hub orchestrating cancer hallmarks through multi-dimensional control networks.Journal of translational medicine · 2025Review
- Triptonide facilitates autophagy-mediated apoptosis in esophageal squamous cell carcinoma by targeting the AMPK-mTOR-ULK1 axis.Acta biochimica et biophysica Sinica · 2025Article
- Gambogic acid suppresses osteosarcoma progression through upregulation of FOXO3a.Discover oncology · 2025Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As one of the hallmarks of cancer, metabolic reprogramming leads to cancer progression, and targeting glycolytic enzymes could be useful strategies for cancer therapy. By screening a small molecule library consisting of 1320 FDA-approved drugs, we found that penfluridol, an antipsychotic drug used to treat schizophrenia, could inhibit glycolysis and induce apoptosis in esophageal squamous cell carcinoma (ESCC). Gene profiling and Ingenuity Pathway Analysis suggested the important role of AMPK in action mechanism of penfluridol. By using drug affinity responsive target stability (DARTS) technology and proteomics, we identified phosphofructokinase, liver type (PFKL), a key enzyme in glycolysis, as a direct target of penfluridol. Penfluridol could not exhibit its anticancer property in PFKL-deficient cancer cells, illustrating that PFKL is essential for the bioactivity of penfluridol. High PFKL expression is correlated with advanced stages and poor survival of ESCC patients, and silencing of PFKL significantly suppressed tumor growth. Mechanistically, direct binding of penfluridol and PFKL inhibits glucose consumption, lactate and ATP production, leads to nuclear translocation of FOXO3a and subsequent transcriptional activation of
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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 Socratic graph.