HIF1A and liver cancer: In addition, it was verified that bruceine D (Bruceine D), by targeting ICAT, blocked the interaction between ICAT and β-catenin, promoted the degradation of β-catenin in liver cancer cells, and then down-regulated HIF-1α and its downstream glucose metabolism expression of related genes in hypoxic liver cancer cells, and ultimately inhibited the energy metabolism of liver cancer cells and the growth of tumors in vivo.