Autophagy, Stress, and Cancer Metabolism: What Doesn't Kill You Makes You Stronger

Cancer cells harbor unique, growth-permissive genetic alterations that deregulate the control of cell growth and proliferation

R. Mathew; E. White

2012

Scholarcy highlights

  • Cancer cells harbor unique, growth-permissive genetic alterations that deregulate the control of cell growth and proliferation
  • The unique metabolism found in human cancers is, to a large extent, a consequence of this deregulation of mTORC1 and its potential impact on the bioenergetic and anabolic demands of rapidly proliferating cancer cells
  • MTORC1 appears to have a more complex role in mitochondrial metabolism because mTORC1 activation promotes mitochondrial biogenesis and oxidative metabolism in some settings and mitochondrial function is important for cancer cell maintenance
  • Human cancer cells with high Ras expression show elevated basal autophagy, which is essential for starvation survival under metabolic stress
  • Targeting autophagy in single-agent therapy to sensitize aggressive cancers that are dependent on autophagy for survival or in combination with therapeutic agents that induce autophagy as a resistance mechanism may be an effective therapeutic strategy
  • A better mechanistic understanding of how autophagy modulates cell metabolism and death signaling under therapeutic stress and how this impacts treatment response will help in developing better therapeutic strategies

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