Snai1, a zinc finger transcription factor, is a master regulator of epithelial-mesenchymal transition (EMT), which is crucial in various biological processes like embryonic development and cancer progression. It is also involved in immune regulation, stem cell properties, and metabolic regulation [2].

In a mouse model, 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 hepatic Snai1 and Snai2 directly promote, via histone modifications, reparative hepatocyte replication and indirectly inhibit liver fibrosis [1]. In triple-negative breast cancer cells, knockout of SNAI1 by Nuclease technology uncovered an epithelio-mesenchymal phenotype accompanied by reduced TGFβ signaling, and the cells gained stemness potential and differentiation plasticity, drifting towards the luminal phenotype [3].

In conclusion, Snai1 is essential in EMT and other biological processes. The gene knockout models in mice have revealed its significance in liver regeneration, fibrosis, and breast cancer cell plasticity. Understanding Snai1's functions provides insights into the mechanisms of disease occurrence and may offer potential therapeutic strategies for liver diseases and breast cancer [1,3].

References:

1. Wang, Pingping, Kang, Qianqian, Wu, Wen-Shu, Rui, Liangyou. 2024. Hepatic Snai1 and Snai2 promote liver regeneration and suppress liver fibrosis in mice. In Cell reports, 43, 113875. doi:10.1016/j.celrep.2024.113875. https://pubmed.ncbi.nlm.nih.gov/38451818/

2. Dong, Bo, Wu, Yadi. 2021. Epigenetic Regulation and Post-Translational Modifications of SNAI1 in Cancer Metastasis. In International journal of molecular sciences, 22, . doi:10.3390/ijms222011062. https://pubmed.ncbi.nlm.nih.gov/34681726/

3. Tsirigoti, Chrysoula, Ali, Mohamad Moustafa, Maturi, Varun, Heldin, Carl-Henrik, Moustakas, Aristidis. 2022. Loss of SNAI1 induces cellular plasticity in invasive triple-negative breast cancer cells. In Cell death & disease, 13, 832. doi:10.1038/s41419-022-05280-z. https://pubmed.ncbi.nlm.nih.gov/36171192/