4.3 Article

Magnolol Induces Apoptosis Through Extrinsic/intrinsic Pathways and Attenuates NF-?B/STAT3 Signaling in Non-small-cell Lung Cancer Cells

Journal

ANTICANCER RESEARCH
Volume 42, Issue 8, Pages 3825-3833

Publisher

INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.15873

Keywords

Key Words; Magnolol; non-small-cell lung cancer; signal transducer and activator of transcription 3; STAT3; nuclear factor kappa B; NF-KB

Categories

Funding

  1. Tainan Municipal Hospital, Tainan, Taiwan [RD-108-03]
  2. Chang Bing Show Chwan Memorial Hospital, Changhua, Taiwan [BRD-109029]
  3. Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan [TTCRD111-13]
  4. Cathay General Hospital, Taipei, Taiwan [CGH-MR-A11013]

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This study found that magnolol, a hydroxylated biphenyl isolated from Magnolia officinalis, has therapeutic effects on non-small-cell lung cancer (NSCLC) by inactivating NF-kappa B signaling and inducing cytotoxicity.
Background/Aim: Non-small-cell lung cancer (NSCLC) is the most common type of lung cancer worldwide, and treatment outcomes are still poor. Magnolol, a hydroxylated biphenyl isolated from Magnolia officinalis, was found to be effective against hepatocellular carcinoma via inactivating nuclear-factor-kappa B (NF-kappa B) signaling. However, whether magnolol targets not only NF-kappa B but also other factors in NSCLC and may contribute to the suppression of tumor progression is unclear. Materials and Methods: Cell viability, flow cytometry, and western blotting assays were used to identify the mechanism of magnolol action in human lung adenocarcinoma cell lines A549 and CL1-5-F4. Results: Our results indicated that magnolol induced cytotoxicity through extrinsic/intrinsic apoptosis

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