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
  • View Affiliations

  • Published online on: October 31, 2017     https://doi.org/10.3892/ol.2017.7303
  • Pages:155-160
  • Copyright: © Feng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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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January 2018
Volume 15 Issue 1

Print ISSN: 1792-1074
Online ISSN:1792-1082

2016 Impact Factor: 1.39
Ranked #68/217 Oncology
(total number of cites)

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Copy and paste a formatted citation
APA
Feng, J., Luo, L., Liu, Y., Fu, S., Chen, J., Duan, X. ... Yang, L. (2018). TP53-induced glycolysis and apoptosis regulator is indispensable for mitochondria quality control and degradation following damage. Oncology Letters, 15, 155-160. https://doi.org/10.3892/ol.2017.7303
MLA
Feng, J., Luo, L., Liu, Y., Fu, S., Chen, J., Duan, X., Xiang, L., Zhang, Y., Wu, J., Fan, J., Wen, Q., Zhang, Y., Yang, J., Peng, J., Zhao, M., Yang, L."TP53-induced glycolysis and apoptosis regulator is indispensable for mitochondria quality control and degradation following damage". Oncology Letters 15.1 (2018): 155-160.
Chicago
Feng, J., Luo, L., Liu, Y., Fu, S., Chen, J., Duan, X., Xiang, L., Zhang, Y., Wu, J., Fan, J., Wen, Q., Zhang, Y., Yang, J., Peng, J., Zhao, M., Yang, L."TP53-induced glycolysis and apoptosis regulator is indispensable for mitochondria quality control and degradation following damage". Oncology Letters 15, no. 1 (2018): 155-160. https://doi.org/10.3892/ol.2017.7303