Galectins (Gals) are evolutionarily conserved proteins that bind to β-galactoside containing glycans. Abnormal expression of Gals is associated with the development, progression, and metastasis of different types of cancer. Among the 11 Gals identified in humans, the roles of Gal-1 and Gal-3 have been extensively investigated in various tumors. Here, we summarize the roles of overly expressed Gal-1 and Gal-3 in the pathogenesis of hepatocellular carcinoma (HCC). The overexpression of Gal-1 and Gal-3 correlates with tumor growth, HCC cell migration and invasion, tumor aggressiveness, metastasis, and poor prognosis. A potentially promising future treatment strategy for HCC may include the combination of immunotherapy with Gal-1 inhibition. Additional research is warranted to investigate targeting Gal-1 and Gal-3 for HCC treatment.
Keywords: Cirrhosis; Epithelial-mesenchymal transition (EMT); Fibrosis; Galectin-1 (Gal-1); Galectin-3 (Gal-3); Hepatocellular carcinoma (HCC); Liver cancer; Metastasis; Non-alcoholic steatohepatitis (NASH).