Effect of liver specific deletion of Zbtb7b on gene expression in liver of mice fasted for 24 hours

Here, we revealed that Zbtb7b is a suppressor of MASLD-related HCC. Zbtb7b deficiency in mouse hepatocytes increases de novo lipogenesis while hepatic fatty acid oxidation is inhibited. Consequently, lipid deposition in the liver is increased, which facilitating the progression of MASLD and eventually to HCC. Mechanistically, depletion of Zbtb7b drastically induced long noncoding RNA H19 expression, thereby driving hepatic de novo lipogenesis and suppressing fatty acid oxidation program to accelerate MASLD-related HCC progression. Overall design: To investigate the role of Zbtb7b in function of liver, we established the Zbtb7b condition knock out mice in liver tissue by injecting Zbtb7bflox/flox mice 1x10^11 AAV2/8-TBG-Cre viral particles via the tail vein.