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6-姜辣素通过调节锰超氧化物歧化酶和细胞外信号调节激酶磷酸化诱导胶质瘤细胞凋亡和细胞周期阻滞。

6-Gingerol Induced Apoptosis and Cell Cycle Arrest in Glioma Cells via MnSOD and ERK Phosphorylation Modulation.

作者信息

Lim Sher-Wei, Chen Wei-Chung, Ko Huey-Jiun, Su Yu-Feng, Wu Chieh-Hsin, Huang Fu-Long, Li Chien-Feng, Tsai Cheng Yu

机构信息

Department of Neurosurgery, Chi-Mei Medical Center, Tainan 702, Taiwan.

Department of Nursing, Min-Hwei College of Health Care Management, Tainan 736, Taiwan.

出版信息

Biomol Ther (Seoul). 2025 Jan 1;33(1):129-142. doi: 10.4062/biomolther.2024.084. Epub 2024 Dec 5.

Abstract

6-gingerol, a bioactive compound from ginger, has demonstrated promising anticancer properties across various cancer models by inducing apoptosis and inhibiting cell proliferation and invasion. In this study, we explore its mechanisms against glioblastoma multiforme (GBM), a notably aggressive and treatment-resistant brain tumor. We found that 6-gingerol crosses the blood-brain barrier more effectively than curcumin, enhancing its potential as a therapeutic agent for brain tumors. Our experiments show that 6-gingerol reduces cell proliferation and triggers apoptosis in GBM cell lines by disrupting cellular energy homeostasis. This process involves an increase in mitochondrial reactive oxygen species (mtROS) and a decrease in mitochondrial membrane potential, primarily due to the downregulation of manganese superoxide dismutase (MnSOD). Additionally, 6-gingerol reduces ERK phosphorylation by inhibiting EGFR and RAF, leading to G1 phase cell cycle arrest. These findings indicate that 6-gingerol promotes cell death in GBM cells by modulating MnSOD and ROS levels and arresting the cell cycle through the ERFR-RAF-1/MEK/ERK signaling pathway, highlighting its potential as a therapeutic agent for GBM and setting the stage for future clinical research.

摘要

6-姜酚是一种来自生姜的生物活性化合物,通过诱导细胞凋亡、抑制细胞增殖和侵袭,在各种癌症模型中都显示出了有前景的抗癌特性。在本研究中,我们探究了其针对多形性胶质母细胞瘤(GBM)的作用机制,GBM是一种极具侵袭性且对治疗耐药的脑肿瘤。我们发现6-姜酚比姜黄素更有效地穿过血脑屏障,增强了其作为脑肿瘤治疗药物的潜力。我们的实验表明,6-姜酚通过破坏细胞能量稳态来减少GBM细胞系中的细胞增殖并触发细胞凋亡。这一过程涉及线粒体活性氧(mtROS)增加和线粒体膜电位降低,主要是由于锰超氧化物歧化酶(MnSOD)下调所致。此外,6-姜酚通过抑制表皮生长因子受体(EGFR)和RAF来降低细胞外信号调节激酶(ERK)磷酸化,导致细胞周期停滞在G1期。这些发现表明,6-姜酚通过调节MnSOD和ROS水平以及通过ERFR-RAF-1/MEK/ERK信号通路使细胞周期停滞来促进GBM细胞死亡,突出了其作为GBM治疗药物的潜力,并为未来的临床研究奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f77d/11704400/681036144ad1/bt-33-1-129-f1.jpg

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