ArticleCarcinogenesis2021
DPYD, down-regulated by the potentially chemopreventive agent luteolin, interacts with STAT3 in pancreatic cancer.
Article in Carcinogenesis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 35 citations in OpenAlex.
- Phytochemicals as Multitarget Therapeutics in Pancreatic Cancer: Mechanisms, Clinical Evidence, and Translational Challenges.Phytotherapy research : PTR · 2026Review
- Dihydropyrimidine dehydrogenase modulates immune response to checkpoint inhibition in mismatch repair deficient/microsatellite instability-high colorectal cancer.Journal for immunotherapy of cancer · 2026Article
- Ellagic acid is associated with reduced pancreatic carcinogenesis and modulation of the IL-6/STAT3 pathway.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026Article
- Current situation and research progress of luteolin in the treatment of gastrointestinal malignant tumors.Discover oncology · 2026Review
- Leveraging the molecular insights and therapeutic potential of diet-derived-flavonoids against pancreatic ductal adenocarcinoma.Frontiers in pharmacology · 2026Review
- Targeting pancreatic cancer with natural compounds: molecular mechanisms, preclinical evidence, clinical perspectives, and limitations.Frontiers in pharmacology · 2026Review
- The mechanism of luteolin suppressing pancreatic cancer (PC) via cyclin B1 (CCNB1)-mediated signalling.Scientific reports · 2025Article
- Updated Review on Natural Polyphenols: Molecular Mechanisms, Biological Effects, and Clinical Applications for Cancer Management.Biomolecules · 2025Review
- Exploring experimental models of prostate cancer in chemoprevention: Oxidative stress as a key pathway to translational research.Pathology international · 2025Review
- Potential anticancer effects and toxicity of flavones luteolin and apigeninJournal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Proteomic profiling of gliomas unveils immune and metabolism-driven subtypes with implications for anti-nucleotide metabolism therapy.Nature communications · 2024Article
- The role of DPYD and the effects of DPYD suppressor luteolin combined with 5-FU in pancreatic cancer.Cancer medicine · 2024Article
- Review
- Unraveling dynamically encoded latent transcriptomic patterns in pancreatic cancer cells by topic modeling.Cell genomics · 2023Article
- Immunopharmacological Activities of Luteolin in Chronic Diseases.International journal of molecular sciences · 2023Review
- Novel Liposomal Formulation of Baicalein for the Treatment of Pancreatic Ductal Adenocarcinoma: Design, Characterization, and Evaluation.Pharmaceutics · 2023Article
- Exploration and Validation of Pancreatic Cancer Hub Genes Based on Weighted Gene Co-Expression Network Analysis and Immune Infiltration Score Analysis.Pharmacogenomics and personalized medicine · 2023Article
- Luteolin, a Potent Anticancer Compound: From Chemistry to Cellular Interactions and Synergetic Perspectives.Cancers · 2022Review
- Plants as a Source of Anticancer Agents: From Bench to Bedside.Molecules (Basel, Switzerland) · 2022Review
- Myocyte enhancer factor 2D promotes hepatocellular carcinoma through AMOTL2/YAP signaling that inhibited by luteolin.International journal of clinical and experimental pathology · 2022Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The 5-year survival rate of pancreatic ductal carcinoma (PDAC) patients is <10% despite progress in clinical medicine. Strategies to prevent the development of PDAC are urgently required. The flavonoids Luteolin (Lut) and hesperetin (Hes) may be cancer-chemopreventive, but effects on pancreatic carcinogenesis in vivo have not been studied. Here, the chemopreventive effects of Lut and Hes on pancreatic carcinogenesis are assessed in the BOP-induced hamster PDAC model. Lut but not Hes suppressed proliferation of pancreatic intraepithelial neoplasia (PanIN) and reduced the incidence and multiplicity of PDAC in this model. Lut also inhibited the proliferation of hamster and human pancreatic cancer cells in vitro. Multi-blot and microarray assays revealed decreased phosphorylated STAT3 (pSTAT3) and dihydropyrimidine dehydrogenase (DPYD) on Lut exposure. To explore the relationship between DPYD and STAT3 activity, the former was silenced by RNAi or overexpressed using expression vectors, and the latter was inactivated by small molecule inhibitors or stimulated by IL6 in human PDAC cells. DPYD knock-down decreased, and overexpression increased, pSTAT3 and cell proliferation. DPYD expression was decreased by inactivation of STAT3 and increased by its activation. The frequency of pSTAT3-positive cells and DPYD expression was significantly correlated and was decreased in parallel by Lut in the hamster PDAC model. Finally, immunohistochemical analysis in 73 cases of human PDAC demonstrated that DPYD expression was positively correlated with the Ki-67 labeling index, and high expression was associated with poor prognosis. These results indicate that Lut is a promising chemopreventive agent for PDAC, targeting a novel STAT3-DPYD pathway.
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