Wu Gong-Jhe, Lin Chien-Ju, Lin Yung-Wei, Chen Ruei-Ming
Department of Anesthesiology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei, Taiwan; Anesthetics and Toxicology Research Center and Department of Anesthesiology, Taipei Medical University Hospital, Taipei, Taiwan.
Graduate Institute of Medical Sciences and Comprehensive Cancer Center, Taipei Medical University, Taipei, Taiwan.
Data Brief. 2016 Oct 8;9:667-672. doi: 10.1016/j.dib.2016.09.045. eCollection 2016 Dec.
This article contains raw and processed data related to a research, "Honokiol induces autophagic cell death in malignant glioma through reactive oxygen species-mediated regulation of the p53/PI3K/Akt/mTOR signaling pathway" (C.J. Lin, T.L. Chen, Y.Y. Tseng, G.J. Wu, M.H. Hsieh, Y.W. Lin, R.M. Chen, 2016) [1]. Data were obtained by immunoblotting analyses of light chain 3 (LC3)-II, beclin-1, Akt, and mTOR in human glioma U87 MG cells and mouse glioma tissues treated with honokiol, an active constituent extracted from the bark of Honokiol induces autophagy of neuroblastoma cells through activating the PI3K/Akt/mTOR and endoplasmic reticular stress/ERK1/2 signaling pathways and suppressing cell migration" (P.S. Yeh, W. Wang, Y.A. Chang, C.J. Lin, J.J. Wang, R.M. Chen, 2016) [2]. The processed data show the effects of honokiol on induction of autophagy in human glioma U87 MG cells by analyzing levels of LC3-II, p62, and bectin-1, "Honokiol-induced apoptosis and autophagy in glioblastoma multiforme cells" (K.H. Chang, M.D Yan, C.J. Yao, P.C. Lin, G.M. Lai, 2013) [3]. In addition, chloroquine, a lysosomal inhibitor, was administered to the cells to further confirm honokiol-induced cell autophagy. Sequentially, mice with gliomas were created and treated with honokiol. Amounts of phosphorylated and non-phosphorylated Akt and mTOR in glioma tissues were analyzed to determine the possible mechanisms of honokiol-induced autophagy.
本文包含与一项研究相关的原始数据和处理后的数据,该研究为“厚朴酚通过活性氧介导的p53/PI3K/Akt/mTOR信号通路调控诱导恶性胶质瘤细胞自噬性死亡”(C.J. 林、T.L. 陈、Y.Y. 曾、G.J. 吴、M.H. 谢、Y.W. 林、R.M. 陈,2016年)[1]。数据通过对用厚朴酚处理的人胶质瘤U87 MG细胞和小鼠胶质瘤组织中的轻链3(LC3)-II、贝克林-1、Akt和mTOR进行免疫印迹分析获得,厚朴酚是从厚朴树皮中提取的一种活性成分。“厚朴酚通过激活PI3K/Akt/mTOR和内质网应激/ERK1/2信号通路并抑制细胞迁移诱导神经母细胞瘤细胞自噬”(P.S. 叶、W. 王、Y.A. 张、C.J. 林、J.J. 王、R.M. 陈,2016年)[2]。处理后的数据通过分析LC3-II、p62和贝汀-1的水平显示了厚朴酚对人胶质瘤U87 MG细胞自噬诱导的影响,“厚朴酚诱导多形性胶质母细胞瘤细胞凋亡和自噬”(K.H. 张、M.D. 严、C.J. 姚、P.C. 林、G.M. 赖,2013年)[3]。此外,向细胞中施用溶酶体抑制剂氯喹以进一步证实厚朴酚诱导的细胞自噬。随后,制备患有胶质瘤的小鼠并用厚朴酚进行治疗。分析胶质瘤组织中磷酸化和非磷酸化Akt和mTOR的量以确定厚朴酚诱导自噬的可能机制。