12-HETE

12-HETE, a major metabolic product of arachidonic acid using 12-LOX catalysis, inhibits cell apoptosis in a dose-dependent manner. 12-HETE promotes the activation and nuclear translocation of NF-κB through the integrin-linked kinase (ILK) pathway^[1].12-HETE has both anti-thrombotic and pro-thrombotic effects^[2]. 12-HETE is a neuromodulator^[3]. In Vitro: 12-HETE participates in the inhibition of cell apoptosis by activating the ILK/NF-κB pathway, implying an important underlying mechanism that promotes the survival of ovarian cancer cells. 12-HETE facilitates cell survival by activating the integrin-linked kinase/NF-κB pathway in ovarian cancer. 12-HETE protects against cell apoptosis in ovarian cancer cells in a concentration-dependent manner. 12-HETE (1 µM) significantly decreases the activation of caspase-3 induced by serum deprivation (SD).12-HETE represses the increased activity of caspase-3 induced by SD in a concentration-dependent manner, with an IC₅₀ value of 1.13 µM^[1].
12-HETE (1 µM) facilitates the activation and nuclear translocation of NF-κB via ILK in ovarian cancer cells^[1].
12-HETE inhibits insulin secretion, reduces metabolic activity and induces cell death in human islets. 12-HETE increases bovine platelet aggregation induced by thrombin and inhibits prostaglandin E1-induced elevation of intracellular cAMP levels. 12-HETE inhibits washed platelet (WP) aggregation^[2].
The neuronal effects of 12-HETE include attenuation of calcium influx and glutamate release as well as inhibition of AMPA receptor (AMPA-R) activation^[3].