| Literature DB >> 27174198 |
Junyang Li1, Chao Tang2, Liwen Li2, Rujun Li3, Youwu Fan4.
Abstract
We previously demonstrated that the acquired resistance because of Hsp27 activation weakens the cytotoxic effect of t-AUCB on glioblastoma cells. Since autophagy is regarded as a survival mechanism for cells exposed to cytotoxic agents, the aim of this study is to investigate whether t-AUCB induces autophagy and whether Hsp27 and autophagy are interacted with each other. Our data demonstrated that t-AUCB induces autophagy in glioblastoma cells and regulates multiple autophagy related-gene expression. t-AUCB induces overexpression of Atg7, which is downstream of Hsp27 and participates in the resistance of glioblastoma cells to t-AUCB treatment. Hsp27 inhibitor quercetin suppresses Atg7 expression and strengthens t-AUCB-induced cell death by autophagy blockage. We concluded that combination of quercetin and t-AUCB might be a potential strategy for glioblastoma treatment.Entities:
Keywords: Autophagy; Glioma; Heat shock protein 27; Quercetin; Soluble epoxide hydrolase inhibitor
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Year: 2016 PMID: 27174198 DOI: 10.1007/s11060-016-2149-2
Source DB: PubMed Journal: J Neurooncol ISSN: 0167-594X Impact factor: 4.130