Sp1, also known as specificity protein 1, is a well-known transcription factor belonging to the Sp family, which also includes Sp2, Sp3 and Sp4 [1]. It activates the transcription of many cellular genes containing CG-rich Sp-binding sites in their promoters and is involved in a variety of essential biological processes such as cell growth, differentiation, apoptosis and carcinogenesis [1]. Sp1 also participates in pathways related to cell proliferation, metastasis, lipid metabolism, inflammation and more, and is of great biological importance [1,2].

In cancer, high levels of Sp1 protein are considered a negative prognostic factor. Compounds that can interfere with Sp1's trans-activating activities may be used in treating tumors that over-express Sp1 [1]. In atherosclerosis, Sp1 is involved in key events like inflammation, lipid metabolism, plaque stability, VSMCs proliferation and endothelial dysfunction [2]. Sp1 also represses distal poly(A) site usage in alternative polyadenylation, and its 3' UTR length regulation in breast cancer may be related to tumorigenic properties [3]. In lung adenocarcinoma, SP1 undergoes phase separation, activates RGS20 expression through super-enhancers, promoting cancer progression, and GSK-J4 can abolish this oncogenic activity [4].

In conclusion, Sp1 is a crucial transcription factor involved in multiple biological processes and various diseases including cancer and atherosclerosis. Understanding its functions through research, although no KO/CKO mouse models are specifically mentioned in the provided references, helps in uncovering the molecular mechanisms of diseases and may provide potential therapeutic targets for these diseases.