Lipid levels within the cells appear to have a role in oncogenesis and inhibition of lipogenic enzymes (such as fatty acid synthase and acetyl-CoA carboxylase) is able to counteract growth of different tumors (Johnson D.L et al. Trends Endocrinol Metab.2016). To date, lipid accumulation and modifications have not been extensively investigated as potential cancer prognostic factors or therapeutic targets in various cancers.
Autophagy, a highly conserved mechanism originally described in yeast, allows the turnover of cellular components and damaged organelles through double-membrane vesicles called autophagosomes, which fuse with lysosomes enabling autophagic substrates degradation by lysosomal enzymes and monomeric units recycle (Liu S et al., Comp Biochem Physiol A Mol Integr Physiol. 2010). Recently the ability of autophagy to mobilize intracellular lipid stores has been described, indicating autophagy modulation as an eligible way to control the amount and the quality of lipids in cancer cells, and several autophagic modulators are already being used in cancer clinical trials. Here, we propose to assess lipidomic networks and changes in the expression of lipid-related and/or autophagy genes in different tumor cell lines (prostate, breast and melanoma cancer cell lines). Moreover, we will evaluate the hypothesis that autophagy modulation might affect lipid composition counteracting tumor growth.
