ArticleMolecular medicine reports2019
Bavachinin exhibits antitumor activity against non‑small cell lung cancer by targeting PPARγ.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- Characterizing risk groups in papillary thyroid carcinoma through T-Cell mediated tumor cell killing-related genes: a pathway to therapeutic predictions.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026Article
- Flavonoids in the Treatment of Non-small Cell Lung Cancer via Immunomodulation: Progress to Date.Molecular diagnosis & therapy · 2025Review
- Exploration potential sepsis-ferroptosis mechanisms through the use of CETSA technology and network pharmacology.Scientific reports · 2025Article
- PPAR-γ in Melanoma and Immune Cells: Insights into Disease Pathogenesis and Therapeutic Implications.Cells · 2025Review
- Exploring the mechanism of rosmarinic acid in the treatment of lung adenocarcinoma based on bioinformatics methods and experimental validation.Discover oncology · 2025Article
- PPARγ Modulators in Lung Cancer: Molecular Mechanisms, Clinical Prospects, and Challenges.Biomolecules · 2024Review
- Exploring the pharmacological aspects of natural phytochemicals against SARS-CoV-2 Nsp14 through an in silico approach.In silico pharmacology · 2023Article
- A bavachinin analog, D36, induces cell death by targeting both autophagy and apoptosis pathway in acute myeloid leukemia cells.Cancer chemotherapy and pharmacology · 2022Article
- Targeting Nuclear Receptors in Lung Cancer-Novel Therapeutic Prospects.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Activation of PPARPPAR research · 2022Article
- Induction of G2/M Cell Cycle Arrest via p38/p21Molecules (Basel, Switzerland) · 2021Article
- PPAR-γ Modulators as Current and Potential Cancer Treatments.Frontiers in oncology · 2021Review
- Potential metabolism determinants and drug-drug interactions of a natural flavanone bavachinin.RSC advances · 2020Article
- Five Constituents inFrontiers in pharmacology · 2019Article
- In vitro Multi-targeted Anti-cancer Effects of Bavachinin in Papillary Thyroid Carcinoma Cell Line: Dual Pathway Inhibition and Cytokine Downregulation.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bavachinin (BNN), one of the main active ingredients of Psoraleacorylifolia, can activate peroxisome proliferator‑activated receptor γ (PPARγ). PPARγ has become a promising therapeutic target in cancer. The aim of the present study was to explore the antitumor effects of BNN in non‑small cell lung cancer (NSCLC). Cell Counting Kit‑8 and lactate dehydrogenase release assays were performed to measure cell toxicity. Western blotting and immunofluorescence were used to analyze the expression of apoptosis‑related factors and PPARγ. The ability of PPARγ to bind to BNN was evaluated by drug affinity responsive target stability (DARTS) and cellular thermal shift assay (CETSA). A reactive oxygen species (ROS) assay kit was used to detect the ROS level. The results revealed that the survival rates and cell viability of A549 cells were reduced by BNN in a dose‑dependent manner. The present results also demonstrated that BNN dose‑dependently changed the expression of Bcl‑2, Bax, caspases‑3/9 and PPARγ. In addition, through the cytotoxic and anti‑proliferative effects, the apoptosis‑related proteins' inhibitive properties of BNN were completely inhibited by the PPARγ antagonists T0070907 and GW9662. The DARTS and CETSA results confirmed the protein binding activity of PPARγ. Furthermore, it was demonstrated that the BNN‑induced ROS generation was dependent on PPARγ activation. Taken together, the present study demonstrated that BNN induced the death of A549 cells by activating PPARγ, an effect mediated by the increased ROS level. These results highlighted the potential role of BNN as a chemotherapeutic agent against NSCLC.
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