Klf3, also known as Kruppel-like factor 3 (basic), is a transcription factor that plays diverse roles in various biological processes. It is involved in adipogenesis, glucose metabolism, epidermal differentiation, and tumor progression, and is associated with pathways such as the WNT/β -catenin and insulin signaling pathways [1-5, 9]. Genetic models, like gene knockout (KO) and conditional knockout (CKO) mouse models, are valuable for studying Klf3's functions.

In skeletal muscle, knockdown of Klf3 promoted basal and insulin-stimulated glucose uptake in L6 myotubes, while overexpression had the opposite effect, indicating its role in insulin sensitivity and glucose metabolism through insulin signal transduction [1]. In epidermal cells, knockdown of Klf3 led to reduced differentiation gene expression, suggesting it is necessary for epidermal differentiation [2]. In colorectal cancer, silencing of Klf3 increased cell proliferation, migration, and invasion, while in gastric cancer, overexpressed Klf3 promoted cell proliferation, migration, invasion, and epithelial-mesenchymal transition, and in lung cancer, KLF3 silencing promoted epithelial-mesenchymal transition and metastasis, showing its complex roles in tumor progression [3,4,5].

In conclusion, Klf3 is a crucial regulator in multiple biological processes. Model-based research, especially KO/CKO mouse models, has revealed its significant contributions to glucose metabolism-related diseases like type 2 diabetes, as well as to cancer development, providing insights into potential therapeutic targets for these diseases.