Non-alcoholic fatty liver disease (NAFLD) is a highly prevalent and slow progressing hepatic pathology characterized by different stages of increasing severity which can ultimately give rise to the development of hepatocellular carcinoma (HCC). Besides drastic lifestyle changes, few drugs are effective to some extent alleviate NAFLD and HCC remains a poorly curable cancer. Among the deregulated molecular mechanisms promoting NAFLD and HCC, several members of the S100 proteins family appear to play an important role in the development of hepatic steatosis, non-alcoholic steatohepatitis (NASH) and HCC. Specific members of this Ca2+-binding protein family are indeed significantly overexpressed in either parenchymal or non-parenchymal liver cells, where they exert pleiotropic pathological functions driving NAFLD/NASH to severe stages and/or cancer development. The aberrant activity of S100 specific isoforms has also been reported to drive malignancy in liver cancers. Herein, we discuss the implication of several key members of this family, e.g., S100A4, S100A6, S100A8, S100A9 and S100A11, in NAFLD and HCC, with a particular focus on their intracellular versus extracellular functions in different hepatic cell types. Their clinical relevance as non-invasive diagnostic/prognostic biomarkers for the different stages of NAFLD and HCC, or their pharmacological targeting for therapeutic purpose, is further debated.

The recombinant antibodies AK247, AK249, AK250, AK280 and AK281 detect by immunohistochemistry the glucagon-secreting alpha cells in mouse pancreatic islets.

The recombinant antibodies AS739, AT693, AU197 and AU734 detect by western blot the spike S protein from SARS-CoV-2.

The recombinant antibodies AS739, AT693 and AU734 detect by immunofluorescence the spike S protein from SARS-CoV-2.

The recombinant antibodies AQ806, AS739, AT693, AU197 and AU734 detect by flow cytometry the spike S protein from SARS-CoV-2.