Genetic screens in yeast have uncovered more than 30 autophagy-related (Atg) genes that are involved in all steps of the autophagic process.4 Most Atg genes are conserved between yeast and mammals, and have very similar functions for autophagy in these organisms. For example, Atg8 and its mammalian homolog LC3 encode ubiquitin-like proteins that are conjugated with lipids in the membranes of the autophagosomes, and its punctate appearance in cells can be used as a marker for autophagosome formation.4 Atg7 is an essential protein for lipidation of Atg8/LC3 and its genetic inactivation is often used to block autophagy.1

Because of its essential biological role, it is not surprising that autophagy is also involved in many pathological conditions, including cancer.1, 2 Although mutations in core Atg genes are rarely found in human cancer,5 autophagy nevertheless influences the outcome of oncogenesis. However, its exact function in cancer is unclear as both tumor-suppressing as well as tumor-promoting activities of autophagy have been reported.1 For example, in epithelial tumor models in the fruit fly Drosophila melanogaster, autophagy is required for tumor growth associated with oncogenic mutations of Ras (RasV12), but it restricts growth of Notch-driven tumors.6 Not only does the oncogene appear to determine the function of autophagy for tumorigenesis, but also the cell type. Activation of autophagy has opposite effects on epithelial vs glia overgrowth induced by expression of YAP/Yorkie, the transcription factor of the Hippo growth control pathway. Epithelial YAP/Yorkie-induced overgrowth can be suppressed by autophagy, while glial overgrowth induced by the same signal is further enhanced by autophagy.6

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