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- 주제어 : Mitochondrial unfolded protein response (검색결과 3 건)
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Chen Hao,Zhang Dong-Ming,Zhang Zhi-Ping,Li Ming-Zhang,Wu Hai-Feng 한국유전학회 2021 Genes & Genomics Vol.43 No.12
Background Mitochondrial unfolded protein response plays an important role in the occurrence and development of breast cancer. However, the role of mitochondrial unfolded protein response (UPRmt) in the sensitivity of breast cancer to cisplatin chemotherapy has not yet been cleared. Objectives The purpose of this study is to explore the role of mitochondrial unfolded protein response in breast cancer sensitivity to cisplatin. Methods In this study, qRT-PCR, Western blotting, Immunofuorescence, CCK-8, Colony formation, Transwell assay and TUNEL staining assay were used to confrm the role of UPRmt in breast cancer cells treated with cisplatin. Results Cisplatin increased the levels of UPRmt including CLPP, HSP60, LONP1 in MCF7 and MDA-MB-231 cells. UPRmt inducer Nicotinamide ribose (NR) could promote the proliferation and invasion of breast cancer cells treated with cisplatin. Importantly, SIRT3 was discovered to increase UPRmt in breast cancer cells and silencing of SIRT3 could inhibit the efect of NR in breast cancer. Conclusions UPRmt regulated by SIRT3 could protect breast cancer cell from cisplatin. Controlling SIRT3-induced UPR may be a potential therapeutic target to increase the sensitivity of breast cancer chemotherapy.
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The mitochondrial unfolded protein response and mitohormesis: a perspective on metabolic diseases
Yi, Hyon-Seung,Chang, Joon Young,Shong, Minho Bioscientifica Ltd 2018 Journal of molecular endocrinology Vol.61 No.3
<P>Mitochondria perform essential roles as crucial organelles for cellular and systemic energy homeostasis, and as signaling hubs, which coordinate nuclear transcriptional responses to the intra- and extra-cellular environment. Complex human diseases, including diabetes, obesity, fatty liver disease and aging-related degenerative diseases are associated with alterations in mitochondrial oxidative phosphorylation (OxPhos) function. However, a recent series of studies in animal models have revealed that an integrated response to tolerable mitochondrial stress appears to render cells less susceptible to subsequent aging processes and metabolic stresses, which is a key feature of mitohormesis. The mitochondrial unfolded protein response (UPR<SUP>mt</SUP>) is a central part of the mitohormetic response and is a retrograde signaling pathway, which utilizes the mitochondria-to-nucleus communication network. Our understanding of the UPR<SUP>mt</SUP> has contributed to elucidating the role of mitochondria in metabolic adaptation and lifespan regulation. In this review, we discuss and integrate recent data from the literature on the present status of mitochondrial OxPhos function in the development of metabolic diseases, relying on evidence from human and other animal studies, which points to alterations in mitochondrial function as a key factor in the regulation of metabolic diseases and conclude with a discussion on the specific roles of UPR<SUP>mt</SUP> and mitohormesis as a novel therapeutic strategy for the treatment of obesity and insulin resistance.</P>
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Avigail T. Erlich,Liam D. Tryon,Matthew J. Crilly,Jonathan M. Memme,Zahra S. Mesbah Moosavi,Ashley N. Oliveira,Kaitlyn Beyfuss,David A. Hood 한국한의학연구원 2016 Integrative Medicine Research Vol.5 No.3
Skeletal muscle mitochondrial content and function are regulated by a number of specialized molecular pathways that remain to be fully defined. Although a number of proteins have been identified to be important for the maintenance of mitochondria in quiescent muscle, the requirement for these appears to decrease with the activation of multiple overlapping signaling events that are triggered by exercise. This makes exercise a valuable therapeutic tool for the treatment of mitochondrially based metabolic disorders. In this review, we summarize some of the traditional and more recently appreciated pathways that are involved in mitochondrial biogenesis in muscle, particularly during exercise.
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