Knockdown of Amphiregulin Triggers Doxorubicin-Induced Autophagic and Apoptotic Death by Regulating Endoplasmic Reticulum Stress in Glioblastoma Cells

doi:10.1007/s12031-020-01598-5

中山醫學大學機構典藏 CSMUIR > 中山醫學大學研究成果 > 期刊論文 > Item 310902500/24897

Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/24897

Title:	Knockdown of Amphiregulin Triggers Doxorubicin-Induced Autophagic and Apoptotic Death by Regulating Endoplasmic Reticulum Stress in Glioblastoma Cells
Authors:	Lee, IN;Yang, JT;Hsieh, MJ;Huang, C;Huang, HC;Ku, YJ;Wu, YP;Huang, KC;Chen, JC
Keywords:	Amphiregulin;Glioblastoma multiforme (GBM);Doxorubicin;Drug resistance;Endoplasmic reticulum (ER) stress;Autophagy
Date:	2020
Issue Date:	2022-08-09T08:09:46Z (UTC)
Publisher:	HUMANA PRESS INC
ISSN:	0895-8696
Abstract:	Glioblastoma multiforme (GBM) is the most common type of malignant brain tumor. The present standard treatment for GBM has not been effective; therefore, the prognosis remains dramatically poor and prolonged survival after treatment is still limited. The new therapeutic strategies are urgently needed to improve the treatment efficiency. Doxorubicin (Dox) has been widely used in the treatment of many cancers for decades. In recent years, with the advancement of delivery technology, more and more research indicates that Dox has the opportunity to be used in the treatment of GBM. Amphiregulin (AREG), a ligand of the epidermal growth factor receptor (EGFR), has been reported to have oncogenic effects in many cancer cell types and is implicated in drug resistance. However, the biological function and molecular mechanism of AREG in Dox treatment of GBM are still unclear. Here, we demonstrate that knockdown of AREG can boost Dox-induced endoplasmic reticulum (ER) stress to trigger activation in both autophagy and apoptosis in GBM cells, ultimately leading to cell death. To explore the importance of AREG in the clinic, we used available bioinformatics tools and found AREG is highly expressed in GBM tumor tissues that are associated with poor survival. In addition, we also used antibody array analysis to dissect pathways that are likely to be activated by AREG. Taken together, our results revealed AREG can serve as a potential therapeutic target and a promising biomarker in GBM.
URI:	http://dx.doi.org/10.1007/s12031-020-01598-5 https://www.webofscience.com/wos/woscc/full-record/WOS:000556445900004 https://ir.csmu.edu.tw:8080/handle/310902500/24897
Relation:	JOURNAL OF MOLECULAR NEUROSCIENCE ,2020 ,v70 ,issue 10 ,p1461-1470
Appears in Collections:	[中山醫學大學研究成果] 期刊論文

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