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Updated: Feb 15, 2026
Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
Published on: July 17, 2018
TP53-induced glycolysis and apoptosis regulator is indispensable for mitochondria quality control and degradation
Jing Feng1, Li Luo2, Yong Liu1
1Department of Oncology, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, P.R. China.
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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