4.2 Article

Accessing Apoptosis Induction and Metastasis Inhibition Effect of Magnolol on Triple Negative Breast Cancer In Vitro

Journal

IN VIVO
Volume 37, Issue 3, Pages 1028-1036

Publisher

INT INST ANTICANCER RESEARCH
DOI: 10.21873/invivo.13177

Keywords

Triple-negative breast cancer; magnolol; extrinsic; intrinsic apoptosis; metastasis; EGFR; JAK; STAT3

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In this study, it was found that magnolol extract from the bark of Magnolia officinalis significantly induced cytotoxicity and apoptosis in TNBC cell lines. It also decreased metastasis and inhibited the EGFR/JAK/STAT3 signaling pathway. Thus, magnolol has the potential to serve as a treatment for TNBC.
Background/Aim: Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer that still requires improvement in treatment. Magnolol extract, derived from the bark of Magnolia officinalis, has traditionally been used in Asia to treat sleeping disorders and anxiety, and as an anti-inflammatory agent. Several reports have indicated that magnolol may have the potential to inhibit the progression of hepatocellular carcinoma and glioblastoma. However, the anti-tumor effect of magnolol on TNBC remains unknown. Materials and Methods: In this study, we used two TNBC cell lines, MDA-MB-231 and 4T1, to examine the cytotoxicity, apoptosis, and metastasis effects of magnolol. These were evaluated using MTT assay, flow cytometry, western blotting, and invasion/migration transwell assay, respectively. Results: Magnolol significantly induced cytotoxicity and extrinsic/intrinsic apoptosis in both TNBC cell lines. It also decreased metastasis and associated protein expression in a dose-dependent manner. Furthermore, the anti-tumor effect was associated with the inactivation of the epidermal growth factor receptor (EGFR)/Janus kinase (JAK)/signal transducer and activator of transcription (STAT3) signaling pathway. Conclusion: Magnolol may not only induce cell death in TNBC through apoptosis signaling activation but also by down-regulating EGFR/JAK/STAT3 signaling, which mediates TNBC progression.

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