FBP1 Controls Liver Cancer Evolution from Senescent MASH Hepatocytes
Introduction:
Hepatocellular carcinoma (HCC) often arises from hepatocytes undergoing compensatory proliferation in livers damaged by metabolic-dysfunction-associated steatohepatitis (MASH). While MASH triggers p53-dependent hepatocyte senescence, the mechanisms bypassing this tumor-suppressive response to enable HCC progression were unclear. This study identifies fructose-1,6-bisphosphatase 1 (FBP1) as a key mediator linking senescence reversal to oncogenic mutagenesis in MASH-driven HCC.
