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Therapeutic strategies targeting these mechanisms may provide novel approaches for GBM treatment by selectively inducing ferroptosis in tumor cells while sparing normal tissues

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FOXO3a from the nucleus to the mitochondria: a round trip in cellular stress response

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doi: 10.1016/j.fbio.2016.04.004

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It appears to be a preferable target due to its overexpression in 80% of TNBC

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mTOR promotes the accumulation of oncometabolites through mitochondrial biogenesis, glutamine metabolism, and HIF-1 signaling

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These characteristics render them an attractive contender for drug delivery applications

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