ArticleMolecules (Basel, Switzerland)2019
Ponatinib Inhibits Proliferation and Induces Apoptosis of Liver Cancer Cells, but Its Efficacy Is Compromised by Its Activation on PDK1/Akt/mTOR Signaling.
Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- ThermoTargetMiner as a proteome integral solubility alteration target database for prospective drugs against lung cancer.Communications chemistry · 2026Article
- The anti-leukemia drug ponatinib attenuates NLRP3 inflammasome activation in macrophages.Immunobiology · 2026Article
- Multi-omics identification of therapeutic targets of compound sappan decoction in hepatocellular carcinoma.Discover oncology · 2026Article
- Integrated Stress Response and Necroptosis Drive Epithelial Dysfunction in Crohn's Disease: Repurposing Cancer Drugs for Permeability Barrier Healing.Gastro hep advances · 2026Article
- Gossypol enhances ponatinib's cytotoxicity against human hepatocellular carcinoma cells by involving cell cycle arrest, p-AKT/LC3II/p62, and Bcl2/caspase-3 pathways.Toxicology reports · 2025Article
- Article
- Cuproptosis-related molecular classification and gene signature of hepatocellular carcinoma and experimental verification.Translational cancer research · 2024Article
- Electrochemical and theoretical studies of the interaction between anticancer drug ponatinib and dsDNA.Scientific reports · 2024Article
- Article
- PTEN-AKT pathway attenuates apoptosis and adverse remodeling in ponatinib-induced skeletal muscle toxicity following BMP-7 treatment.Physiological reports · 2023Article
- DepLink: an R Shiny app to systematically link genetic and pharmacologic dependencies of cancer.Bioinformatics advances · 2023Article
- The Landscape of PDK1 in Breast Cancer.Cancers · 2022Review
- Receptor-Tyrosine Kinase Inhibitor Ponatinib Inhibits Meningioma Growth In Vitro and In Vivo.Cancers · 2021Article
- The Risk of Arterial Thrombosis in Patients With Chronic Myeloid Leukemia Treated With Second and Third Generation BCR-ABL Tyrosine Kinase Inhibitors May Be Explained by Their Impact on Endothelial Cells: An In-Vitro Study.Frontiers in pharmacology · 2020Article
- Article
- Sodium cantharidate targets STAT3 and abrogates EGFR inhibitor resistance in osteosarcoma.Aging · 2019Article
- HIF-1α Regulates Glucocorticoid-Induced Osteoporosis Through PDK1/AKT/mTOR Signaling Pathway.Frontiers in endocrinology · 2019Article
- Tanshinone IIA Reverses Oxaliplatin Resistance In Human Colorectal Cancer Via Inhibition Of ERK/Akt Signaling Pathway.OncoTargets and therapy · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Ponatinib is a multi-target protein tyrosine kinase inhibitor, and its effects on hepatocellular carcinoma cells have not been previously explored. In the present study, we investigated its effects on hepatocellular carcinoma cell growth and the underlying mechanisms. Toward SK-Hep-1 and SNU-423 cells, ponatinib induces apoptosis by upregulation of cleaved caspase-3 and -7 and promotes cell cycle arrest in the G1 phase by inhibiting CDK4/6/CyclinD1 complex and phosphorylation of retinoblastoma protein. It inhibits the growth-stimulating mitogen-activated protein (MAP) kinase pathway, the phosphorylation of Src on both negative and positive regulation sites, and Jak2 and Stat3 phosphorylation. Surprisingly, it also activates the PDK1, the protein kinase B (Akt), and the mechanistic target of rapamycin (mTOR) signaling pathway. Blocking mTOR signaling strongly sensitizes cells to inhibition by ponatinib and makes ponatinib a much more potent inhibitor of hepatocellular carcinoma cell proliferation. These findings demonstrate that ponatinib exerts both positive and negative effects on hepatocellular cell proliferation, and eliminating its growth-stimulating effects by drug combination or potentially by chemical medication can significantly improve its efficacy as an anti-cancer drug.
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Registered trials
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