TP53-induced glycolysis and apoptosis regulator is indispensable for mitochondria quality control and degradation following damage

Mitochondria have been described as 'the powerhouse of the cell' as the organelle generates the majority of adenosine triphosphate (ATP) in cells to support life. Mitochondria can be damaged due to stress, for example by reactive oxygen species (ROS). TP53-induced glycolysis and apoptosis...

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Bibliographic Details
Published in:Oncology letters 2018-01, Vol.15 (1), p.155-160
Main Authors: Feng, Jing, Luo, Li, Liu, Yong, Fu, Shaozhi, Chen, Jie, Duan, Xiaoxia, Xiang, Li, Zhang, Yanling, Wu, Jinbo, Fan, Juan, Wen, Qinglian, Zhang, Ye, Yang, Jingpin, Peng, Jinxia, Zhao, Ming, Yang, Linglin
Format: Article
Language:English
Subjects:
Adenosine triphosphate
Apoptosis
Autophagy
Biotechnology
Cell regulation
Cytochrome
Genetic aspects
Health aspects
Kinases
Laboratories
Metabolic disorders
Microscopy
Mitochondria
Mitochondrial DNA
Physiology
Proteins
Quality control
Reactive oxygen species
Studies
Tumor proteins
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Summary:Mitochondria have been described as 'the powerhouse of the cell' as the organelle generates the majority of adenosine triphosphate (ATP) in cells to support life. Mitochondria can be damaged due to stress, for example by reactive oxygen species (ROS). TP53-induced glycolysis and apoptosis regulator (TIGAR) serves a role in suppressing ROS damage and may protect mitochondria integrity. In the present study, the localization of TIGAR on mitochondria in 5-8F cells was demonstrated. Furthermore, it was indicated that the knockdown of TIGAR using lentivirus-short hairpin RNA induces the loss of mitochondrial membrane potential and cytochrome c leakage. However, these damaged mitochondria were not degraded in cells, but exhibited an abnormal appearance as indicated by mitochondrial swelling, crista collapse and vacuolization, with physiological dysfunction marked by reduced ATP production. Therefore, TIGAR maybe an indispensable protein for mitochondrial protection and degradation following cellular damage.
ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2017.7303