Journal
AUTOPHAGY
Volume 14, Issue 8, Pages 1467-1468Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2018.1475819
Keywords
Apoptosis; autophagy; CRISPR/Cas9; FOXO3; homeostasis; MDM2; PUMA; transcription
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Funding
- NIH [RO1CA150925, RO1CA190170]
- National Institutes of Health [RO1CA150925, RO1CA190170]
- NATIONAL CANCER INSTITUTE [R01CA150925, R01CA190170] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007635] Funding Source: NIH RePORTER
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The molecular machinery linking macroautophagy (autophagy hereafter) to apoptosis is still being elucidated. A recent study found that the transcription factor FOXO3/FOXO3A (forkhead box O3), which regulates autophagy, is itself regulated by basal autophagy to determine apoptosis sensitivity. Autophagy inhibition confers cell sensitivity to anti-cancer agents, and this effect is explained by the ability of FOXO3 to transactivate the pro-apoptotic gene BBC3/PUMA. Here, we discuss the possibility that FOXO3 acts as a cell surveillance mechanism to correct autophagy perturbations (i.e., autophagy inhibition), and confers apoptosis sensitization if this autophagy imbalance is not rectified.
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