Senescence is engaged in response to oncogenes to suppress proliferation. Cancers rewire metabolism to facilitate proliferation; however, it is not well appreciated how this enables senescence bypass. Recent work by Buj et al. demonstrates that loss of the tumor suppressor p16 engages a mTORC1-dependent increase in nucleotide pools to override senescence.
Keywords: RPIA; mTORC1; nucleotide metabolism; p16; pentose phosphate pathway.
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