Cudraflavone B induces human glioblastoma cells apoptosis via ER stress-induced autophagy

被引:7
作者
Pan, Jinlin [1 ,2 ]
Zhao, Rongchuan [1 ,2 ]
Dong, Caihua [1 ,2 ]
Yang, Jiao [3 ]
Zhang, Ruobing [2 ]
Sun, Minxuan [2 ]
Ahmad, Nafees [4 ]
Zhou, Yuanshuai [1 ,2 ]
Liu, Yanxiang [5 ]
机构
[1] Univ Sci & Technol China, Sch Biomed Engn Suzhou, Div Life Sci & Sci & Med, Hefei 230026, Peoples R China
[2] Chinese Acad Sci, Suzhou Inst Biomed Engn & Technol, Jiangsu Key Lab Med Opt, Keling Rd 88, Suzhou 215163, Peoples R China
[3] Suzhou Sci & Technol Town Hosp, Inst Clin Med Res, Suzhou 215153, Peoples R China
[4] Inst Biomed & Genet Engn, Islamabad, Pakistan
[5] Suzhou Sci & Technol Town Hosp, Dept Pathol, 1 Li Jiang Rd, Suzhou 215153, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
GBM; Endoplasmic reticulum stress; Unfolded protein response; Autophagy; ENDOPLASMIC-RETICULUM; GROWTH-INHIBITION; DEATH;
D O I
10.1186/s12868-023-00778-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
BackgroundGlioblastoma (GBM) is the most common malignant intracranial tumor with a low survival rate. However, only few drugs responsible for GBM therpies, hence new drug development for it is highly required. The natural product Cudraflavone B (CUB) has been reported to potentially kill a variety of tumor cells. Currently, its anit-cancer effect on GBM still remains unknown. Herein, we investigated whether CUB could affect the proliferation and apoptosis of GBM cells to show anti-GBM potential.ResultsCUB selectively inhibited cell viability and induced cell apoptosis by activating the endoplasmic reticulum stress (ER stress) related pathway, as well as harnessing the autophagy-related PI3K/mTOR/LC3B signaling pathway. Typical morphological changes of autophagy were also observed in CUB treated cells by microscope and scanning electron microscope (SEM) examination. 4-Phenylbutyric acid (4-PBA), an ER stress inhibitor, restored the CUB-caused alteration in signaling pathway and morphological change.ConclusionsOur finding suggests that CUB impaired cell growth and induced cell apoptosis of glioblastoma through ER stress and autophagy-related signaling pathways, and it might be an attractive drug for treatment of GBM.
引用
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页数:10
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