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    Pyrogallol Suppresses the Tumor Progression

    Hao Liu1, Yanxiang Chang1, Lei Jin1 Corresponding author

    1. 1Department of Cardiothoracic Surgery, The First Affiliated Hospital of Xi’an Medical University, Xi’an, Shaanxi Province, China.

    CORRESPONDENCE

    Lei Jin

    Department of Cardiothoracic Surgery, The First Affiliated Hospital of Xi’an Medical University, Xi’an, Shaanxi Province, China.

    jinlei2024@sina.com

    Received: 19-01-2024; Accepted: 05-03-2024.

    Volume 20, Issue 3 · pp. 973–982 · PUBLISHED 2024 · DOI: 10.1177/09731296241242542

    View on Pharmacogn. Mag. original site ↗

    ABSTRACT

    Background: Pyrogallol, a bioactive compound derived from natural sources, is the focus of this study, aiming to investigate its anti-cancer properties against A549 lung cancer cells and uncover the underlying mechanisms. Purpose: This study seeks to elucidate the therapeutic potential of pyrogallol as a novel anti-cancer agent for NSCLC by targeting aerobic glycolysis and signal transducer and activator of transcription 2 (STAT2) signaling pathway. Background: Pyrogallol, a bioactive compound derived from natural sources, is the focus of this study, aiming to investigate its anti-cancer properties against A549 lung cancer cells and uncover the underlying mechanisms. Materials and Methods: A range of pyrogallol doses was administered to A549 cells, followed by a comprehensive analysis utilizing bioinformatic tools like Gene Expression Omnibus (GEO), GEO2R, WebGestalt, and the Search Tool for Interactions of Chemicals database. Assessments of cytotoxicity were conducted using 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide (MTT) and trypan blue assays post-treatment of A549 cells with pyrogallol. Cell cycle progression and cell death were evaluated via flow cytometry using Annexin V-fluorescein isothiocyanates/propidium iodide double staining. Network analysis helped identify pertinent signaling pathways, while RT-PCR validated mRNA expression changes in A549 cells. Auto dock docking studies were employed to gauge the binding affinity of pyrogallol with targets associated with the STAT2-mediated pathway. Results: Pyrogallol notably impeded the progression of A549 cells by prompting cell cycle arrest in the G0/G1 phase and fostering apoptosis. Network analysis highlighted its role in regulating metabolism, apoptosis, and STAT2 targets linked to lung tumorigenesis. RT-PCR validation affirmed the downregulation of genes associated with cell cycle and apoptosis targets. Furthermore, docking studies indicated a robust binding affinity between pyrogallol and the signaling targets within the STAT2 pathway. Pyrogallol displays the potential to halt the growth of lung cancer cells, indicating its promise as a viable treatment for this condition. Conclusion: These discoveries emphasize the need for additional research and clinical studies to fully harness its therapeutic benefits for lung cancer treatment.

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      Liu, H., Chang, Y., & Jin, L. (2024). Pyrogallol Suppresses the Tumor Progression. Pharmacognosy Magazine, 20(3), 973–982. https://doi.org/10.1177/09731296241242542