Autophagy, a highly conserved and tightly regulated catabolic process, is thought to have both pro-tumor and anti-tumor functions. Several studies have elucidated mechanisms explaining tumor suppres-sive roles for autophagy. However, significantly less is known about the mechanisms mediating autophagy's pro-tumor functions beyond its role in promoting survival in response to stress. In particular, how autophagy, a key pathway proposed to sustain core metabolic functions during starvation or stress, contributes to oncogenic transformation, remains unknown. This matter harbors particular significance in the context of strong oncogenic insults, namely Ras activation, because they coor-dinately drive tumor cell proliferation and alter metabolic pathways within the cancer cell to meet with enhanced energy and biosynthetic demands. Recently, we discovered that autophagy promotes Ras transformation, which we propose is due to a previously unrecognized role for autophagy in facilitating proliferation and glycolytic metabolism during oncogenic transformation.
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