Abstract
Abstract DJ-1 is involved in many key cellular processes including cell proliferation, transcriptional regulation, differentiation, oxidative stress protection, and mitochondrial function maintenance. Deregulation of DJ-1 has been implicated in the pathogenesis of many human diseases such as Parkinson's disease, amyotrophic lateral sclerosis, infertility, and cancer. DJ-1 was initially identified as an oncogene product involved in human tumorigenesis in numerous cancer types. Alteration in expression of DJ-1 is associated with tumorigenesis in several types of cancers. Herein, we aimed to clarify the effect of DJ-1 on stemness and radioresistance of glioma stem cells (GSCs). Firstly, we found that the reduction in expression of DJ-1 in brain tumor tissues when compared with tumor adjacent normal brain tissues, as indicated by reduced DJ-1 staining. Knock-down of DJ-1 inhibited self-renewal activity of GSCs in vitro as evidenced by neurosphere formation, limiting dilution, and soft agar clonogenic assays. DJ-1 knock-down suppressed maintenance of stemness by suppressing the expression of Notch intracellular domain, Sox2, and phosphorylated STAT3 proteins. Intriguingly, DJ-1 knock-down inhibited the expression of EGFRvIII in GSCs which might be the cause of suppression of stemness pathways. In addition, knockdown of DJ-1 induced apoptosis, reduced cell invasiveness, and sensitized GSCs to ionizing radiation. Based on these data, we propose that DJ-1 could be considered as a crucial diagnostics and therapeutics target for malignant glioma. Note: This abstract was not presented at the meeting. Citation Format: Myung-Jin Park, Jeong-Yub Kim, Hee-Jin Kim, Ji-Soo Kim, Jeong-Chul Kim, Dea-Hee Lee, Yoo-Jin Na. Dj-1 confers maintenance of stemness and radioresistance by regulating EGFRvIII expression in glioma stem cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 2879. doi:10.1158/1538-7445.AM2017-2879
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