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In addition, inhibition of SLC7A11, genetically or pharmacologically, has been shown to result in cellular defects typically associated with oncogenic pathway inactivation, including suppression of cell proliferation/growth and invasion, defective clonogenic survival, and decreased anchorage-independent growth, whereas SLC7A11 overexpression can exert the opposite cellular effects (Ishimoto et al., 2011
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Cancer cells enhance mTORC1 activity, which promotes gene transcription and protein synthesis to control cell proliferation, metabolism, and autophagy [72,73,74]
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