دورية أكاديمية
أعرض في EDS

NRBF2-mediated autophagy contributes to metabolite replenishment and radioresistance in glioblastoma.

التفاصيل البيبلوغرافية
العنوان: NRBF2-mediated autophagy contributes to metabolite replenishment and radioresistance in glioblastoma.
المؤلفون: Kim J; Department of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea., Kang H; Department of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea., Son B; siRNAgen Therapeutics, Daejeon, 34302, Republic of Korea., Kim MJ; Nuclear Science Research Institute, Pusan National University, Busan, 46241, Republic of Korea.; Department of Naval Architecture and Ocean Engineering, Pusan National University, Busan, 46241, Republic of Korea., Kang J; Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, USA., Park KH; Department of Chemistry, Pusan National University, Busan, 46241, Republic of Korea.; SoulDot Co., Ltd, Pusan National University, Busan, 46241, Republic of Korea., Jeon J; Department of Radiation Oncology, Haeundae Paik Hospital, Inje University School of Medicine, Busan, 48108, Republic of Korea., Jo S; Department of Radiation Oncology, Haeundae Paik Hospital, Inje University School of Medicine, Busan, 48108, Republic of Korea., Kim HY; Department of Neurosurgery, Haeundae Paik Hospital, Inje University College of Medicine, Busan, 48108, Republic of Korea., Youn H; Department of Integrative Bioscience and Biotechnology, Sejong University, Seoul, Republic of Korea. hsyoun@sejong.ac.kr., Youn B; Department of Integrated Biological Science, Pusan National University, Busan, 46241, Republic of Korea. bhyoun72@pusan.ac.kr.; Department of Biological Sciences, Pusan National University, Busan, Republic of Korea. bhyoun72@pusan.ac.kr.
المصدر: Experimental & molecular medicine [Exp Mol Med] 2022 Nov; Vol. 54 (11), pp. 1872-1885. Date of Electronic Publication: 2022 Nov 04.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: United States NLM ID: 9607880 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2092-6413 (Electronic) Linking ISSN: 12263613 NLM ISO Abbreviation: Exp Mol Med Subsets: MEDLINE
أسماء مطبوعة: Publication: Jan. 2013- : New York : Nature Publishing Group
Original Publication: Seoul : Korean Society of Medical Biochemistry and Molecular Biology, 1996-
مواضيع طبية MeSH: Autophagy* , Autophagy-Related Proteins*/metabolism , Brain Neoplasms*/drug therapy , Brain Neoplasms*/metabolism , Brain Neoplasms*/radiotherapy , Glioblastoma*/drug therapy , Glioblastoma*/metabolism , Glioblastoma*/radiotherapy , Trans-Activators*/metabolism , Radiation Tolerance*, Animals ; Humans ; Mice ; Cell Line, Tumor ; Cell Survival ; Disease Models, Animal ; Lidoflazine/therapeutic use
مستخلص: Overcoming therapeutic resistance in glioblastoma (GBM) is an essential strategy for improving cancer therapy. However, cancer cells possess various evasion mechanisms, such as metabolic reprogramming, which promote cell survival and limit therapy. The diverse metabolic fuel sources that are produced by autophagy provide tumors with metabolic plasticity and are known to induce drug or radioresistance in GBM. This study determined that autophagy, a common representative cell homeostasis mechanism, was upregulated upon treatment of GBM cells with ionizing radiation (IR). Nuclear receptor binding factor 2 (NRBF2)-a positive regulator of the autophagy initiation step-was found to be upregulated in a GBM orthotopic xenograft mouse model. Furthermore, ATP production and the oxygen consumption rate (OCR) increased upon activation of NRBF2-mediated autophagy. It was also discovered that changes in metabolic state were induced by alterations in metabolite levels caused by autophagy, thereby causing radioresistance. In addition, we found that lidoflazine-a vasodilator agent discovered through drug repositioning-significantly suppressed IR-induced migration, invasion, and proliferation by inhibiting NRBF2, resulting in a reduction in autophagic flux in both in vitro models and in vivo orthotopic xenograft mouse models. In summary, we propose that the upregulation of NRBF2 levels reprograms the metabolic state of GBM cells by activating autophagy, thus establishing NRBF2 as a potential therapeutic target for regulating radioresistance of GBM during radiotherapy.
(© 2022. The Author(s).)
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المشرفين على المادة: 0 (Autophagy-Related Proteins)
0 (Trans-Activators)
0 (NRBF2 protein, human)
J4ZHN3HBTE (Lidoflazine)
تواريخ الأحداث: Date Created: 20221105 Date Completed: 20221213 Latest Revision: 20221228
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC9723115
DOI: 10.1038/s12276-022-00873-2
PMID: 36333468
قاعدة البيانات: MEDLINE
الوصف
تدمد:2092-6413
DOI:10.1038/s12276-022-00873-2