Metabolic reprogramming in hepatocellular carcinoma: mechanisms and therapeutic implications

Abstract

Hepatocellular carcinoma features extensive metabolic reprogramming. This includes alterations in major biochemical pathways such as glycolysis, the pentose phosphate pathway, amino acid metabolism and fatty acid metabolism. Moreover, there is a complex interplay among these altered pathways, particularly involving acetyl-CoA (coenzyme-A) metabolism and redox homeostasis, which in turn influences reprogramming of other metabolic pathways. Understanding these metabolic changes and their interactions with cellular signaling pathways offers potential strategies for the targeted treatment of hepatocellular carcinoma and improved patient outcomes. This review explores the specific metabolic alterations observed in hepatocellular carcinoma and highlights their roles in the progression of the disease. Cancer cells often change their metabolism to support rapid growth. This study examines how liver cancer, specifically hepatocellular carcinoma (HCC), alters its metabolism and explores potential treatments. The authors focus on how HCC cells use glucose, amino acids and fatty acids differently from normal cells. HCC cells rely heavily on glycolysis even when oxygen is present, a phenomenon known as the Warburg effect. They also activate the pentose phosphate pathway to produce molecules needed for growth and survival. Additionally, HCC cells depend on certain amino acids such as glutamine and serine for building blocks and energy. This study highlights that targeting these altered metabolic pathways could be a promising strategy for treating HCC. In conclusion, understanding these metabolic changes in HCC can lead to new treatment approaches. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.