Cancer cells harbor unique, growth-permissive genetic alterations that deregulate the control of cell growth and proliferation
2012
Key concepts
- cell growth
- von Hippel –Lindau
- tumor suppressor
- extracellular matrix
- phosphoinositide 3-kinase
- succinate dehydrogenase
- fumarate hydratase
- glycolysis
- cancer cell
- aggressive cancer
- PDK1
- metabolism
- reactive oxygen species
- autophagy
- GLUT1
- electron transport chain
- receptor tyrosine kinases
- mitochondria
- synthesis
- C. elegans
- chemotherapy
- therapeutic agent
- tricarboxylic acid
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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