Abstract
Primary liver cancer is the fourth leading cause of cancer death around the world. Histologically, it can be divided into two major groups, hepatocellular carcinoma (75% of all liver cancer) and intrahepatic cholangiocarcinoma (15% of all liver cancer) [1, 2]. Primary liver cancer usually happens in liver disease or cirrhosis patients [1], and the risk factors for developing HCC depend on the etiology [3] and the country of provenance [1]. There is an urgent need for an accurate diagnostic test given the high proportion of false positives and false negatives for alpha-fetoprotein (AFP), a common HCC biomarker [4]. Due to often being diagnosed in advanced stages, HCCrelated deaths per year have doubled since 1999 [3]. With the use of metabolomics technologies [5], the aberrant metabolism characteristics of cancer tissues can be discovered and exploited for the new biomarkers and new therapies to treat HCC [6, 7].
Highlights
Primary liver cancer is the fourth leading cause of cancer death around the world
Primary liver cancer usually happens in liver disease or cirrhosis patients [1], and the risk factors for developing hepatocellular carcinoma (HCC) depend on the etiology [3] and the country of provenance [1]
The study led by Xu et al has revealed the crucial role of liver receptor homolog 1 (LRH-1) in regulating mitochondrial glutamine metabolism, which eventually leads to the production of NADPH through a noncanonical glutamine pathway
Summary
Different oncogenic mutations lead to different metabolic phenotypes in primary liver cancer. MYC and MET mutations regulate glucose and glutamine metabolism differently in primary liver cancer. Glucose metabolism increased by acetylated phosphoglycerate kinase 1 (PGK1) leads to the promotion of cancer cell proliferation and tumorigenesis in the liver. There exist metabolic differences between hepatocellular carcinoma (HCC) and normal liver tissue or other liver diseases
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