Figure 1.

Intra- and intercellular fatty acid trafficking in starved cells and in the tumor microenvironment. (A) We showed that in starved cells with impaired mitochondrial fusion (mitofusin 1 knockout [Mfn1 KO] and optic atrophy 1 knockout [Opa1 KO]), fragmented mitochondria received highly variable amounts of fatty acids (FAs). These FAs were not efficiently metabolized, resulting in increased FA storage within lipid droplets (LDs) and transfer of FAs to neighboring wild-type (WT) cells. (B) This is analogous to a 2-compartment model of tumor metabolism, in which upregulated autophagy, fragmentation of mitochondria, or increased lipolysis in supporting host cells promotes tumor growth, presumably through intercellular transfer of FAs. Numbers in parentheses refer to references. Oxphos., oxidative phosphorylation; DRAM, damage-regulated autophagy modulator; Mff, mitochondrial fission factor.