Fosl1, also known as Fos-like antigen 1, is a component of AP1 transcription factor complexes. It plays a crucial role in cell differentiation and tumorigenesis, controlling processes like epithelial-mesenchymal transformation in solid tumors [4]. It is also involved in regulating various signaling pathways, such as the UBC9/CYLD/NF-κB axis [1].

In glioblastoma stem cells, knocking down FOSL1 in mesenchymal (MES) subtype cells leads to loss of MES features and tumor-initiating ability, while ectopic expression in proneural (PN) subtype cells induces PN-to-MES transition (PMT) [1]. In head and neck squamous cell carcinoma, depletion of FOSL1 disrupts super-enhancers and suppresses tumor initiation and metastasis [2]. In proximal tubular cells of the kidney, selective Fosl1 deficiency (Fosl1Δtub) increases the severity of cisplatin-or folate-induced acute kidney injury (AKI), as characterized by lower kidney function, more severe inflammation, and Klotho downregulation [3]. In a genetically engineered mouse (GEM) model of cholangiocarcinoma, FOSL1 genetic abrogation extended mouse survival by decreasing the oncogenic potential of transformed cholangiocytes [5].

In conclusion, Fosl1 is an important regulator in processes such as cell differentiation, tumorigenesis, and tissue injury response. Studies using gene knockout (KO) or conditional knockout (CKO) mouse models have revealed its significant roles in diseases like glioblastoma, head and neck squamous cell carcinoma, AKI, and cholangiocarcinoma, providing potential therapeutic targets for these diseases.