ArticleInternational journal of molecular sciences2022
Chrysin-Induced G Protein-Coupled Estrogen Receptor Activation Suppresses Pancreatic Cancer.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 2 of them syntheses that pooled it.
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Who cites it
14 citing papers in PubMed, 2 syntheses or guidelines pooled it, 20 citations in OpenAlex.
- Intricate roles of estrogen and estrogen receptors in digestive system cancers: a systematic review.Cancer biology & medicine · 2024Pooled it
- A large-scale, observational study to investigate the current status of diabetes complication and their prevention in Japan: incidence/risk factors for malignancies during follow-up-JDCP study 11 (English version).Diabetology international · 2024Guideline
- Exploratory Proteomic Profiling Reveals Potential Mediators of 5-FU Response under p53 Deficiency in Colon Cancer Cells.Biomolecules & therapeutics · 2026Article
- Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative Review.International journal of molecular sciences · 2025Review
- Article
- Anticancer Activity of Ether Derivatives of Chrysin.Molecules (Basel, Switzerland) · 2025Review
- New insights into Notch signaling as a crucial pathway of pancreatic cancer stem cell behavior by chrysin-polylactic acid-based nanocomposite.Discover oncology · 2025Review
- Review
- The Pros and Cons of Estrogens in Prostate Cancer: An Update with a Focus on Phytoestrogens.Biomedicines · 2024Review
- Therapeutic potential of flavonoids from traditional Chinese medicine in pancreatic cancer treatment.Frontiers in nutrition · 2024Review
- Advancements and recent explorations of anti-cancer activity of chrysin: from molecular targets to therapeutic perspective.Exploration of targeted anti-tumor therapy · 2024Review
- Natural products as inhibitors against pancreatic cancer cell proliferation and invasion: possible mechanisms.American journal of cancer research · 2024Review
- Molecular Diagnostics, Pathology and Biomarkers of Gastrointestinal Neoplasms.International journal of molecular sciences · 2023Article
- The current status and future of PD-L1 in liver cancer.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Pancreatic cancer (PC) has a high mortality rate due to its poor prognosis and the possibility of surgical resection in patients with the disease. Importantly, adjuvant chemotherapy is necessary to improve PC prognosis. Chrysin, a natural product with anti-inflammatory, antioxidant, and anticancer properties, has been studied for several years. Our previous study demonstrated that chrysin induced G protein-coupled estrogen receptor (GPER) expression and regulated its activity in breast cancer. Herein, we investigated whether chrysin-induced GPER activation suppresses PC progression in MIA PaCa-2 cells and a xenograft model. To determine its mechanism of action, cytotoxicity and clonogenic assays, a FACS analysis, and Western blotting were performed. Furthermore, the delay in tumor growth was evaluated in the MIA PaCa-2-derived xenograft model. Tumor tissues were investigated by Western blotting, immunohistochemistry, and a proteomic analysis. Chrysin caused cell cycle arrest and significantly decreased cell viability. Following co-treatment with chrysin and 17β-estradiol, the inhibitory effect of chrysin on cell proliferation was enhanced. In the xenograft model, chrysin and G1 (a GPER agonist) significantly delayed tumor growth and reduced both Ki-67 (a proliferation marker) and c-Myc expressions in tumor tissues. The proteomic analysis of tumor tissues identified that rho-associated coiled-coil containing protein kinase 1 (ROCK1), transgelin 2 (TAGLN2), and FCH and Mu domain containing endocytic adaptor 2 (FCHO2) levels were significantly reduced in chrysin-treated tumor tissues. High
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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.