厚朴酚通过外源性/内源性途径诱导非小细胞肺癌细胞凋亡，并抑制 NF-κB/STAT3 信号通路。

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

机构信息

Division of Hematology/Oncology, Department of Internal Medicine, Tainan Municipal Hospital (Managed by Show Chwan Medical Care Corporation), Tainan, Taiwan, R.O.C.

Department of Biological Science and Technology, China Medical University, Taichung, Taiwan, R.O.C.

出版信息

Anticancer Res. 2022 Aug;42(8):3825-3833. doi: 10.21873/anticanres.15873.

DOI:10.21873/anticanres.15873

PMID:35896265

Abstract

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-B) signaling. However, whether magnolol targets not only NF-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 signaling and suppressed phosphorylation of signal transducer and activator of transcription 3 (STAT3)/NF-B and expression of their downstream proteins.

CONCLUSION

Magnolol not only induced extrinsic and intrinsic apoptosis signaling but also inactivated STAT3/NF-B and attenuated their signaling of epithelial-mesenchymal transition and metastasis-related protein expression in NSCLC.

摘要

背景/目的：非小细胞肺癌（NSCLC）是全球最常见的肺癌类型，其治疗效果仍不理想。从厚朴中分离得到的羟基联苯厚朴酚，通过抑制核因子-κB（NF-κB）信号通路，被发现对肝癌有效。然而，厚朴酚是否不仅针对 NF-κB，而且还针对 NSCLC 中的其他因素，并可能有助于抑制肿瘤进展尚不清楚。