Autophagy is a highly regulated-cell pathway for degrading long-lived proteins 
as well as for clearing cytoplasmic organelles. Autophagy is a key contributor 
to cellular homeostasis and metabolism. Warburg hypothesized that cancer growth 
is frequently associated with a deviation of a set of energy generation 
mechanisms to a nonoxidative breakdown of glucose. This cellular phenomenon 
seems to rely on a respiratory impairment, linked to mitochondrial dysfunction. 
This mitochondrial dysfunction results in a switch to anaerobic glycolysis. It 
has been recently suggested that epithelial cancer cells may induce the Warburg 
effect in neighboring stromal fibroblasts in which autophagy was activated. 
These series of observations drove to the proposal of a putative reverse Warburg 
effect of pathophysiological relevance for, at least, some tumor phenotypes. In 
this review we introduce the autophagy process and its regulation and its 
selective pathways and role in cancer cell metabolism. We define and describe 
the Warburg effect and the newly suggested "reverse" hypothesis. We also discuss 
the potential value of modulating autophagy with several pharmacological agents 
able to modify the Warburg effect. The association of the Warburg effect in 
cancer and stromal cells to tumor-related autophagy may be of relevance for 
further development of experimental therapeutics as well as for cancer 
prevention.