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

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

doi:10.3892/ol.2017.7303

January-2018 Volume 15 Issue 1

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January-2018 Volume 15 Issue 1

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Article Open Access

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

Authors:
- Jing Feng
- Li Luo
- Yong Liu
- Shaozhi Fu
- Jie Chen
- Xiaoxia Duan
- Li Xiang
- Yanling Zhang
- Jinbo Wu
- Juan Fan
- Qinglian Wen
- Ye Zhang
- Jingpin Yang
- Jinxia Peng
- Ming Zhao
- Linglin Yang
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Affiliations: Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China, Department of Laboratory Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China, Department of Rheumatology and Immunology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China, Department of Anesthesiology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China, Department of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China

Copyright: © Feng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 155-160
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Published online on: October 31, 2017

https://doi.org/10.3892/ol.2017.7303
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Abstract

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.

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Journals

International Journal of Molecular Medicine

International Journal of Oncology

Molecular Medicine Reports

Oncology Reports

Experimental and Therapeutic Medicine

Oncology Letters

Biomedical Reports

Molecular and Clinical Oncology

World Academy of Sciences Journal

International Journal of Functional Nutrition

International Journal of Epigenetics

Medicine International

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

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