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Fatty acid synthase (FASN) is a key enzyme that plays a critical role innumerous metabolic functions by catalyzing the synthesis for long-chain fattyacids. FASN is highly expressed in various human cancers. This preferential expressionmakes FASN an attractive target for anticancer therapy. Hexokinase II (HKII) isoverexpressed in most cancer cells, and it generally localizes to the outer mitochondrialmembrane. Recent studies have demonstrated the protective role of mitochondrialHKII in preservation of mitochondrial integrity. The association of hexokinasewith mitochondria has emerged as a powerful mechanism in protecting numerous celltypes against cell death. We performed this study to examine the mechanism underlyingapoptosis induced by cerulenin and with specific focus on its effect on HKII inZR-75-1 human breast cancer cells. Additionally, we sought to elucidate whetherinhibition of the PI3K/Akt pathway can potentiate the anticancer effect of cerulenin.Here, we showed that cerulenin disrupts the physical association between HKIIand AIF, leading to eventual cell death. In addition, LY294002, a PI3K/Akt inhibitor,sensitized ZR-75-1 breast cancer cells to cerulenin-induced apoptosis. Collectively,cerulenin induces apoptosis via disrupting the interaction between AIF and HKIIand inhibition of PI3K sensitizes cells to cerulenin-induced apoptosis in ZR-75-1cells.

Cerulenin-induced apoptosis is mediated by disrupting the interaction between AIF and hexokinase II