Sestrin 2 protects against metabolic stress in a p53-independent manner
| Autor: | Jing Yan, Jia Sun, Zhen-Xian Du, Bao-Qin Liu, Jing-Yi Jiang, Hua-Qin Wang, Jia-Mei Wang, Chao Li |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
RNA Stability Biophysics Biology medicine.disease_cause Biochemistry Mice 03 medical and health sciences Transactivation 0302 clinical medicine Stress Physiological Cell Line Tumor P53 status medicine Animals RNA Messenger Metabolic Stress Molecular Biology Mutation Nuclear Proteins Cell Biology Adaptive response Cell biology Glucose 030104 developmental biology Cytoprotection 030220 oncology & carcinogenesis Cancer cell Tumor Suppressor Protein p53 Adaptation Oxidative stress |
| Zdroj: | Biochemical and Biophysical Research Communications. 513:852-856 |
| ISSN: | 0006-291X |
| Popis: | Glucose limitation activates p53, which functions as an adaptive response to maintain cell survival. However, p53 is frequently deleted or mutated in a variety of tumors, while most cancer cells can acclimatize themselves to metabolically unfavorable surrounding, indicating that alternative mechanisms other than p53 transactivation underly adaptive response of cancer cells with p53 deletion or mutation to metabolically hostile environment. Sestrin 2 (SESN2) is a p53 downstream target, which plays a protective role against various stressful stimuli, such as genotoxic, energetic, and oxidative stress. In the current study, we demonstrated that SESN2 transcript was stabilized by glucose limitation at the posttranscriptional level irrespective of p53 status. Importantly, SESN2 also protected cells from metabolic stress triggered by glucose limitation in a p53-independent manner. Our data indicated that stabilization of SESN2 transcript might be an alternative adaptive response to metabolic stress other than p53 activation. Thereby, the current study highlights the significance of stabilization of SESN2 transcript in adaptation of cells with p53 deletion or mutation to metabolic stress. |
| Databáze: | OpenAIRE |
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