A functional switch of Galectin-1: A glycan-dependent driver of liver cancer progression.

The progression of hepatocellular carcinoma (HCC) from chronic hepatitis to fibrosis and malignancy is considered to be critically driven by the dynamic reprogramming of the cell-surface "glyco-code". The endogenous lectin Galectin-1 (Gal-1) recognizes these glycan signals, yet a unifying framework for understanding its pleiotropic roles has been lacking. Here, we propose a core regulatory concept: Gal-1 acts as a "decoder" for the evolving glyco-code, and this process determines its functional outputs. We systematically characterize the stage-specific functional shifts of Gal-1 in liver disease: it serves as a double-edged immunomodulator during hepatitis, acts as a core driver of fibrosis progression, and ultimately functions as a multifunctional pro-tumorigenic factor in established HCC. This "glyco-code interpreter" model offers a new perspective on the complexities of chronic hepatic injury and may provide a theoretical basis for developing novel therapeutic strategies that target this key regulatory framework.