Klf12-flox Mouse

Klf12, known as Krüppel-like factor 12, is a transcriptional regulator. It belongs to the Kruppel-like factor family of transcription factors that bind to DNA, RNA, and proteins, regulating gene transcription [5]. Klf12 has been implicated in various biological processes, including angiogenesis, neural tube development, and NK cell proliferation [1].

In esophageal squamous cell carcinoma (ESCC), Klf12 down-regulation promotes cisplatin resistance and cancer metastasis. Mechanistically, Klf12 binds to the L1CAM promoter to repress its expression, and the E3 ubiquitin ligase TRIM27 ubiquitinates Klf12, affecting its transcriptional activity [1].

In non-small cell lung cancer (NSCLC), Klf12 binds to the PD-L1 promoter to promote its transcription, and in immunocompetent mice, Klf12 knockout inhibits tumor growth and promotes CD8+ T cell infiltration [2].

In breast cancer, Klf12 promotes cell proliferation by inhibiting the p53/p21 axis both in a p53-dependent and p53-independent manner [3].

In male mice, KLF12 aggravates angiotensin II-induced cardiac remodeling by transcriptionally inhibiting SMAD7 [4].

In human airway epithelial cells, KLF12 inhibits lipopolysaccharide-induced inflammatory responses, oxidative stress, pyroptosis, and endoplasmic reticulum stress through the NF-κB pathway [6].

In conclusion, Klf12 is a crucial transcriptional regulator involved in multiple biological processes and diseases. Gene knockout and other functional studies in mouse models have revealed its roles in cancer metastasis, drug resistance, tumor immunity, cardiac remodeling, and inflammatory responses. Understanding Klf12 provides insights into disease mechanisms and potential therapeutic targets for cancers, cardiac diseases, and asthma-related conditions.