Autophagy activation and SREBP-1 induction contribute to fatty acid metabolic reprogramming by leptin in breast cancer cellsIF4.5

Autophagy, an intracellular self-digestive process forremoving damaged cytoplasmic constituents, has beenshown to play a role in modulation of cancer cell survival and proliferation [22]. Recently, there has beenan increasing appreciation of the contribution of thiscomplex process to cancer cell-specific metabolicchanges [23]. In certain tumor types, autophagy maypromote tumor growth by providing tumor cells withdiverse metabolic fuel sources such as glucose, aminoacids, nucleosides, and fatty acid. However, the directinvolvement of autophagy in lipid metabolism wasunder-evaluated until a novel function of autophagy,termed as lipophagy, was discovered [24]. Accordingly,autophagy is essentially required for lipid dropletbreakdown and thus plays a key role in release of freefatty acid (FFA) from storage sites. Hence, it is notsurprising that inhibition of autophagy flux impedeslipid metabolism in cancer cells, which in turn leads toa reduction in energy production and cell proliferation[25,26]. On the contrary, other studies have alsoreported that autophagy is implicated in lipid synthesisand accumulation [27,28], suggesting a complicated
and context-dependent role of autophagy in cancercell-specific lipid metabolism.Although leptin has been well known to supporttumor growth through multiple mechanisms [3,6,29],little effort has been made to examine the variousmetabolic effects in cancer cells and its potential rolesin the pro-carcinogenic effects of this adipokine.

感谢延南大学细胞培养研究所引用文献