Linking Glycogen and Senescence in Cancer Cells

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Linking Glycogen and Senescence in Cancer Cells Susana Ros, Almut Schulze Cell Metabolism Volume 16, Issue 6, Pages 687-688 (December 2012) DOI: 10.1016/j.cmet.2012.11.010 Copyright © 2012 Elsevier Inc. Terms and Conditions

Figure 1 Overview of Glycogen Metabolism in Cancer Cells Exposed to Hypoxia and Effects of PYGL Depletion Favaro et al. report the induction of several enzymes involved in glycogen synthesis (blue) and degradation (red) in cancer cells under hypoxic conditions. Channeling of glucose through glycogen promotes the survival of cancer cells under hypoxia. Depletion of PYGL reduces glycogen mobilization and impairs NADPH production due to decreased flux through the PPP, resulting in ROS accumulation and induction of senescence. Branching enzyme 1, GBE1; glucose transporter 1, GLUT1; glycogen phosphorylase liver isoform, PYGL; glycogen synthase muscle isoform, GYS1; glucose-1-phosphate, Glc-1-P; glucose-6-phosphate, Glc-6-P; hexokinase II, HK-II; phosphoglucomutase 1, PGM-1; pentose phosphate pathway, PPP; reactive oxygen species, ROS; UDP-glucose, UDP-Glc. Cell Metabolism 2012 16, 687-688DOI: (10.1016/j.cmet.2012.11.010) Copyright © 2012 Elsevier Inc. Terms and Conditions