ArticleCancer science2010
Cantharidin, a potent and selective PP2A inhibitor, induces an oxidative stress-independent growth inhibition of pancreatic cancer cells through G2/M cell-cycle arrest and apoptosis.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 2 of them syntheses that pooled it.
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Who cites it
92 citing papers in PubMed, 2 syntheses or guidelines pooled it, 183 citations in OpenAlex.
- Bibliometric Analysis and Systemic Review of Cantharidin Research Worldwide.Current pharmaceutical biotechnology · 2024Pooled it
- Efficacy and safety of sodium cantharidinate and vitamin B6 injection for the treatment of digestive system neoplasms: a meta-analysis of randomized controlled trials.Drug design, development and therapy · 2019Pooled it
- Venom-Derived Enzyme Inhibitors as Anticancer Agents: Structure-Activity Relationships, Molecular Targets and Mechanistic Insights.Molecules (Basel, Switzerland) · 2026Review
- Transcriptomics, Proteomics and Network Pharmacology Reveal the Mechanisms of Cantharidin-Induced Kidney Injury in Rats.Current issues in molecular biology · 2026Article
- A novel approach to combatMicrobiology spectrum · 2026Article
- PP2Acα regulates cerebellar development via phosphorylation-dependent neuronal programs.iScience · 2026Article
- Uncovering cantharidin's mechanism for cholangiocarcinoma treatment using patient-derived tumor organoids.iScience · 2025Article
- PP2A Promotes the Symmetric Division of MUC1-Dominant Cancer Stem-Like Cells in Small Cell Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Off-label use of sodium cantharidinate and vitamin B6 injection in cancer: a protocol for a systematic review and meta-analysis.Systematic reviews · 2025Article
- Norcantharidin inhibits TOP2A expression via H3K27me3 mediated epigenetic regulation to alleviate the progression of hepatocellular carcinoma.Frontiers in pharmacology · 2025Article
- Cantharidin overcomes IL-2Rα signaling-mediated vorinostat resistance in cutaneous T-cell lymphoma through reactive oxygen species.Journal for immunotherapy of cancer · 2024Article
- Article
- PP2A Affects Angiogenesis via Its Interaction with a Novel Phosphorylation Site of TSP1.International journal of molecular sciences · 2024Article
- p300 nucleocytoplasmic shuttling underlies mTORC1 hyperactivation in Hutchinson-Gilford progeria syndrome.Nature cell biology · 2024Article
- Altering phosphorylation in cancer through PP2A modifiers.Cancer cell international · 2024Review
- Integrative analysis of the molecular signature of target genes involved in the antitumor effects of cantharidin on hepatocellular carcinoma.BMC cancer · 2023Article
- Hepatotoxic mechanism of cantharidin: insights and strategies for therapeutic intervention.Frontiers in pharmacology · 2023Review
- Inhibition of MZF1/c-MYC Axis by Cantharidin Impairs Cell Proliferation in Glioblastoma.International journal of molecular sciences · 2022Article
- Bioactive constituents of animal-derived traditional Chinese medicinal materials for breast cancer: opportunities and challenges.Journal of Zhejiang University. Science. B · 2022Review
- Combination of dasatinib and okadaic acid induces apoptosis and cell cycle arrest by targeting protein phosphatase PP2A in chronic myeloid leukemia cells.Medical oncology (Northwood, London, England) · 2022Article
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cantharidin is an active constituent of mylabris, a traditional Chinese medicine. It is a potent and selective inhibitor of protein phosphatase 2A (PP2A) that plays an important role in control of cell cycle, apoptosis, and cell-fate determination. Owing to its antitumor activity, cantharidin has been frequently used in clinical practice. In the present study, we investigated the therapeutic potential of cantharidin in pancreatic cancer. Cantharidin efficiently inhibited the growth of pancreatic cancer cells, but presented a much lighter toxicity effect against normal pancreatic duct cells. It caused G2/M cell-cycle arrest that was accompanied by the down-regulation of cyclin-dependent kinase 1 (CDK1) and up-regulation of p21 expression. It induced apoptosis and elevated the expressions of pro-apoptotic factors tumor necrosis factor-alpha (TNF-alpha), TNF-related apoptosis inducing receptor 1 (TRAILR1), TRAILR2, Bad, Bak, and Bid, and decreased the expression of anti-apoptotic Bcl-2. Activation of caspase-8 and caspase-9 suggested that both extrinsic and intrinsic pathways are involved in the induction of apoptosis. Interestingly, unlike previous studies on other cancer cells, we found that the inhibitory role of cantharidin is independent of oxidative stress in pancreatic cancer cells. Mitogen-activated protein kinases (MAPKs), including ERK, JNK, and p38, were activated after treatment with cantharidin. Inhibition of JNK, but not ERK or p38, alleviated the cytotoxity effect of cantharidin, suggesting cantharidin exerted its anticancer effect through the JNK-dependent way. Hence, in addition to being an attractive candidate compound with therapeutic potential, cantharidin also highlighted the possibility of using PP2A as a therapeutic target for pancreatic cancer treatment.
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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.