Snai1, a zinc finger transcription factor, is a master regulator of epithelial-mesenchymal transition (EMT) [2]. It also drives various cancer-related processes such as cell invasion, survival, immune regulation, stem cell properties, and metabolic regulation [2]. Snai1's regulation occurs at transcriptional, translational, and predominantly post-translational levels like phosphorylation, acetylation, and ubiquitination [2].

In liver-related studies, hepatocyte-specific deletion of both Snai1 and Snai2 (but not one alone) suppresses liver cyclin A2/D1 expression and regenerative hepatocyte proliferation after hepatectomy or CCl4 treatments, while augmenting CCl4-stimulated HSC activation and liver fibrosis. This indicates that Snai1, along with Snai2, promotes liver regeneration and suppresses liver fibrosis, likely via histone modifications [1]. In breast cancer stem cells, stable overexpression of Snai1 in MCF-7 cells induced the expression of EMT-related genes, increased migration, invasion, and in vitro tumorigenesis. SnaI1 positively regulated genes like ALCAM, MMP2, MMP13, MMP14, VCAN, ANKRD1, KRT16, CTGF, TGFRIIβ, PROCR, and negatively regulated CDH1, DSP, and DSC3B, leading to EMT [3].

In summary, Snai1 is crucial in EMT and various cancer-related processes. Its functions in liver regeneration and fibrosis, as well as in breast cancer stem cell-related EMT, are revealed through gene-knockout-based studies. These findings help in understanding the mechanisms of diseases like liver fibrosis and cancer, providing potential targets for therapeutic intervention.