ArticleThe Journal of biological chemistry2012
Isorhamnetin inhibits proliferation and invasion and induces apoptosis through the modulation of peroxisome proliferator-activated receptor γ activation pathway in gastric cancer.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 68 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
68 citing papers in PubMed, 139 citations in OpenAlex.
- The possible role of sirtuins and MiRNAs in gastrointestinal cancers: special focus on Sirt1.Cancer cell international · 2026Review
- Progress in the antitumor molecular mechanisms of Isorhamnetin.Discover oncology · 2025Review
- Isorhamnetin: Reviewing Recent Developments in Anticancer Mechanisms and Nanoformulation-Driven Delivery.International journal of molecular sciences · 2025Review
- Unveiling the therapeutic potential of HZQYF: exploring the inhibitory impact of a clinical herbal formula on gastric cancer through network pharmacology and transcript analysis.BMC complementary medicine and therapies · 2025Article
- From Traditional Efficacy to Drug Design: A Review of Astragali Radix.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Exploring the pharmacokinetics, drug-likeness, and toxicological features of anticancer flavonoids: a Boulevard to explore their clinical translational potential.Frontiers in pharmacology · 2025Review
- Isorhamnetin: what is theFrontiers in pharmacology · 2024Review
- Comparative analysis of flavonoid metabolites from different parts of Hemerocallis citrina.BMC plant biology · 2023Article
- Natural compounds targeting nuclear receptors for effective cancer therapy.Cancer metastasis reviews · 2023Review
- Isorhamnetin exerts anti-tumor activity in DEN + CClMedical oncology (Northwood, London, England) · 2023Article
- Demystifying the Functional Role of Nuclear Receptors in Esophageal Cancer.International journal of molecular sciences · 2022Review
- Isorhamnetin Suppresses Human Gastric Cancer Cell Proliferation through Mitochondria-Dependent Apoptosis.Molecules (Basel, Switzerland) · 2022Article
- Escaping mechanisms of ESKAPE pathogens from antibiotics and their targeting by natural compounds.Biotechnology reports (Amsterdam, Netherlands) · 2022Article
- Targeting Nuclear Receptors in Lung Cancer-Novel Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Anticancer applications of phytochemicals in gastric cancer: Effects and molecular mechanism.Frontiers in pharmacology · 2022Review
- Application of Quercetin in the Treatment of Gastrointestinal Cancers.Frontiers in pharmacology · 2022Review
- Baohuoside I Inhibits Tumor Angiogenesis in Multiple MyelomaFrontiers in pharmacology · 2022Article
- Impact of Phytochemicals on PPAR Receptors: Implications for Disease Treatments.PPAR research · 2022Review
- EditingInternational journal of molecular sciences · 2021Review
- Enzymatic Metabolism of Flavonoids by Gut Microbiota and Its Impact on Gastrointestinal Cancer.Cancers · 2021Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 5 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is a lethal malignancy and the second most common cause of cancer-related deaths. Although treatment options such as chemotherapy, radiotherapy, and surgery have led to a decline in the mortality rate due to GC, chemoresistance remains as one of the major causes for poor prognosis and high recurrence rate. In this study, we investigated the potential effects of isorhamnetin (IH), a 3'-O-methylated metabolite of quercetin on the peroxisome proliferator-activated receptor γ (PPAR-γ) signaling cascade using proteomics technology platform, GC cell lines, and xenograft mice model. We observed that IH exerted a strong antiproliferative effect and increased cytotoxicity in combination with chemotherapeutic drugs. IH also inhibited the migratory/invasive properties of GC cells, which could be reversed in the presence of PPAR-γ inhibitor. We found that IH increased PPAR-γ activity and modulated the expression of PPAR-γ regulated genes in GC cells. Also, the increase in PPAR-γ activity was reversed in the presence of PPAR-γ-specific inhibitor and a mutated PPAR-γ dominant negative plasmid, supporting our hypothesis that IH can act as a ligand of PPAR-γ. Using molecular docking analysis, we demonstrate that IH formed interactions with seven polar residues and six nonpolar residues within the ligand-binding pocket of PPAR-γ that are reported to be critical for its activity and could competitively bind to PPAR-γ. IH significantly increased the expression of PPAR-γ in tumor tissues obtained from xenograft model of GC. Overall, our findings clearly indicate that antitumor effects of IH may be mediated through modulation of the PPAR-γ activation pathway in GC.
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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 OpenQuestion graph.