Krt19, also known as Keratin 19, is a type I cytokeratin that forms the intermediate filament cytoskeleton and is crucial for maintaining epithelial cell structure [3,4]. It has been associated with various biological processes and disease-related pathways. For example, it is involved in cell-cycle regulation, cell death, and pathways like Wnt/β-catenin, epithelial-mesenchymal transition (EMT), and immune-related processes [2,3,4,5].

In a mouse model, multiplexed genome editing of hepatocytes in vivo demonstrated that Krt19 promoted liver tumorigenesis. Krt19 knockout markedly enhanced histone acetylation levels as it promotes CoREST complex formation, increasing histone deacetylase activity. This indicates its role in liver cancer dedifferentiation through epigenetic regulation [1]. In pancreatic cancer, overexpression of Krt19 boosted cell proliferation, migration, and invasion. Hypoxia-induced upregulation of Krt19, along with loss of miR-642a-5p, favored cancer progression [2]. In thyroid cancer, knockdown of Krt19 inhibited the proliferation and migration of cancer cell lines, suggesting its role in promoting metastasis via EMT [5].

In conclusion, Krt19 plays essential roles in maintaining epithelial cell integrity and is involved in multiple disease-related processes. Gene-knockout studies in mice, especially in liver, pancreatic, and thyroid cancer models, have revealed its significant impact on tumorigenesis, metastasis, and epigenetic regulation, providing valuable insights into the mechanisms of these diseases and potential therapeutic targets.