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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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[1]

Western Blot Analysis[1]