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Updated: Jul 7, 2026

Measuring mRNA Levels Over Time During the Yeast S. cerevisiae Hypoxic Response
Published on: August 10, 2017
Translational repression during chronic hypoxia is dependent on glucose levels
Jeff D Thomas1, Lizalynn M Dias, Gregg J Johannes
1Department of Pathology and Laboratory Medicine, Drexel University College of Medicine, Philadelphia, Pennsylvania 19102, USA.
Hypoxia represses translation, but only when glucose is depleted. Adding glucose or oxygen restores translation, revealing a dual requirement for translational control in cancer cells.
Area of Science:
- Cellular Biology
- Cancer Research
- Biochemistry
Background:
- Hypoxia is common in solid tumors and often leads to translational repression.
- Previously, prolonged hypoxia (>16 hours) was thought to be the sole trigger for this repression.
Purpose of the Study:
- To investigate the role of glucose availability in hypoxia-induced translational repression.
- To elucidate the mechanism underlying translational inhibition under combined glucose and oxygen deprivation.
Main Methods:
- Utilized PC3 cell lines under varying conditions of hypoxia and glucose availability.
- Monitored translation rates, glucose levels, and eukaryotic initiation factor 2-alpha (eIF2alpha) phosphorylation.
- Assessed the involvement of pancreatic eIF2alpha kinase (PERK) in the observed effects.
Main Results:
- Prolonged hypoxia leads to glucose depletion, which correlates with translation shutdown.
- Glucose addition or reoxygenation restored translation in hypoxic cells, indicating both factors are necessary.
- eIF2alpha phosphorylation was reversed by glucose, and this process was independent of PERK.
Conclusions:
- Glucose depletion, not just hypoxia, is essential for translational repression.
- This finding explains the prolonged exposure requirement for hypoxia-induced translational inhibition.
- Understanding the glucose-hypoxia interplay is crucial for comprehending solid tumor growth and metabolism.
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