De novo lipogenesis is elicited dramatically in human hepatocellular carcinoma especially in hepatitis C virus-induced hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is the third leading cause of cancer deaths worldwide. Abnormal de novo lipogenesis is reported to be involved in hepatocarcinogenesis. In current study, de novo lipogenesis and its association with patient survival rate were investigated in human HCC samples induced by hepatitis B virus (HBV), hepatitis C virus (HCV), or nonviral factors.

Inhibition of Autophagy Prolongs Recipient Survival Through Promoting CD8 T Cell Apoptosis in a Rat Liver Transplantation Model.

In liver transplantation (LT), although various immunosuppressants have been used in clinical practice, acute rejection remains a common complication that significantly shortens recipient survival. In recent years, manipulating immune tolerance has been regarded as one of the promising solutions to rejection. Autophagy, an evolutionarily conserved protein degradation system, has been reported to be involved in immune rejection and may be a target to establish immune tolerance.

The cytoskeleton protein β-actin may mediate T cell apoptosis during acute rejection reaction after liver transplantation in a rat model.

Cytoskeletal proteins and associated regulatory proteins are essential for maintaining cell structure and growth. β-actin is a major component of the cytoskeleton, and β-actin remodeling is involved in lymphocyte migration, infiltration and apoptosis. However, little is known about whether changes in β-actin expression affect lymphocyte cell fate, particularly during acute rejection after liver transplantation in a rat model.