On April 18, 2018, a paper named “Squalene epoxidase drives NAFLD-induced hepatocellular carcinoma and is a pharmaceutical target” published on the journal of Science Translational Medicine. The researchers performed RNA-seq analysis of 17 paired NAFLD-HCC tumor and adjacent normal tissues. They found that among up-regulated metabolic genes, SQLE was a top outlier gene and it was overexpressed in 16 of 17 paired NAFLD-HCC samples, so they did the experiment for SQLE.

    It is reported that SQLE locates in the microsomes of the endoplasmic reticulum. With the help of the action of molecular oxygen and reduced coenzyme II, SQLE can catalyze the conversion of squalene to epoxidized squalene. The epoxidized squalene is an intermediate product for the conversion of squalene to lanosterol. And lanosterol is a precursor in the process of the conversion of squalene to cholesterol in the body, which illustrates the important role of SQLE in cholesterol production. Via a series of cell and animal experiments, the researchers found that overexpression of SQLE would promote the accumulation of cholesteryl esters in liver cells and increase the level of oxidative stress. The increase in oxidative stress levels would lead to the change of the level of intracellular methylation which would activate The PTEN/AKT/mTOR signaling pathway thus promoted the occurrence and growth of liver cancer.

    The research team then used terbinafine to suppress the level of SQLE and further validated their experimental results. This research provides a new experimental basis and direction for the prevention and treatment of NAFLD-related liver cancer.

    Welcome to choose and buy the product SQLE protein, SQLE antibody or SQLE kit.