Proteomic heterogeneity reveals SOAT1 as a potential biomarker for hepatocellular carcinoma

Liver cancer is one of the few and fastest neoplastic malignancy to continue to rise in incidence in the United States and across the world (1). Today, the 5-year survival rate of liver cancer is approximately 17%, making it the 2nd most common cause of death from cancer worldwide (2). A highly heterogeneous disease, hepatocellular carcinoma (HCC) is the more common subtype of liver cancer and research lacks information on the prominent drivers that promote disease progression leading to limited therapeutic options. However, common yet diverse risk factors have been identified that promote tumors heterogeneity which include Hepatitis B or C viral infection, liver flukes, diet, and alcohol. Together, these factors lead to cirrhosis of the liver, ultimately putting individuals at risk of developing liver cancer. Because there is a sequential nature of the onset of HCC with liver cirrhosis as the main risk factor, scientists and clinicians have sought to determine if HCC can be detected at an early stage of carcinogenesis before advancing to the later, more deadly stage of disease. Advances in omic-based technologies have made tremendous efforts in unmasking genotypic and phenotypic features of HCC such as transcriptomics, genomics, metabolomics, and proteomics. While these approaches give in depth analyses of tumors with multiple and diverse cellular pathways coming forward as contributors of cancer development, it is difficult to parse through which gene hits are the key players of hepatocarcinogenesis to further validate in functional studies