Magnolol is a phenolic compound extracted from magnolia officinalis, exhibited anti-tumor potential against many types of cancers. Magnolol has also recognized as an anti-inflammation agent which can downregulate several inflammation signals transduction. Glioblastoma multiforme (GBM) is the most common central nervous system (CNS) tumor and associated with poor prognosis among adults due to rapid growth and aggressive invasion. However, the treatment efficacy of current standard therapy for GBM is remaining unsatisfied. Nevertheless, whether magnolol may suppress GBM progression and its underlying mechanism has not been elucidated. Thus, the purpose of this study was to investigate the mechanism and therapeutic efficacy of magnolol on GBM.First of all, we validated the potential treatment targets of GBM with the GEPIA (Gene Expression Profiling Interactive Analysis) analysis and Western blotting assay. GEPIA data indicated the PKCδ/STAT3 signaling pathway as a potential target of GBM that may affect patient survival. In our results, magnolol can effectively suppress the phosphorylation and the nuclear translocation of STAT3 in GBM cells. Then, we used the MTT assay to investigate the cytotoxicity of GBM cells after various dose of magnolol treatment. We also detected the extrinsic/intrinsic apoptosis induction ability of magnolol on GBM cells. This study also demonstrated that magnolol may significantly trigger the loss of mitochondrial membrane potential, and the activation of cleaved caspase-3, -8 and -9. Transwell invasion and wound healing assays was used to identify the suppression of migration and invasion effects of magnolol on glioblastoma cells. Meanwhile, tumor invasion and migration ability and the associated genes, including MMP9 and uPA, were all diminished by magnolol treatment. In sum, our results demonstrated that magnolol suppressed GBM progression may be associated with the inactivation of PKCδ/STAT3 signaling transduction. Citation Format: Sin-Rong Lee, Yuan Chang, I-Tsang Chiang, Fei-Ting Hsu. Magnolol induces apoptosis and inhibits invasion ability via suppression of STAT3 signaling in glioblastoma multiforme cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 5392.

Magnolol is a phenolic compound extracted from magnolia officinalis, and known as a common Chinese medicinal material used in the treatment of strokes, colds, etc. Magnolol has also recognized as an anti-inflammation agent which can downregulate several inflammation signals transduction. Several reports suggested that magnolol may also have anti-tumor potential in liver and colon cancer. Nevertheless, the regulatory mechanism of magnolol on apoptosis and NF-κB signaling in human bladder cancer has not been elucidated. Thus, the purpose of the study was to investigate the mechanism and therapeutic efficacy on bladder cancer. First of all, we used MTT assay to investigate the cytotoxicity induction after magnolol treatment in bladder cancer. Then, we used NF-κB translocation assay to evaluate whether the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) was decreased after magnolol treatment. We also detected the apoptosis induction ability of magnolol on extrinsic/intrinsic apoptosis pathway. This study demonstrated that magnolol significantly triggered the accumulation at the sub-G1 phase, the loss of mitochondrial membrane potential, and the activation of cleaved caspase-3, -8 and -9. Further verify the effect of magnolol on the expression of anti-apoptotic related proteins, we performed Western blotting. Magnolol inhibited migration and invasion ability of bladder cancer were investigated by wound healing and invasion assay. Then, we performed Western blotting to detect whether magnolol may inhibit NF-κB-mediated downstream signaling that involving in anti-apoptosis and metastasis such as MCL-1 and MMP9 protein expression. Moreover, the reduction of Cyclin D1 protein expression was used to evaluate the inhibition of cell proliferation by magnolol. In sum, our result demonstrated that magnolol induced extrinsic and intrinsic apoptosis mechanism and inhibit invasion/migration ability of bladder cancer was associated with the inactivation of NF-κB. Citation Format: Sin-Rong Lee, Zhao-Lin Tan, Yuan Chang, I-Tsang Chiang, Fei-Ting Hsu. Magnolol induces apoptosis and inhibits metastasis via suppression of NF-κB activation in human bladder cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 978.

No abstract