Foxq1, a member of the large forkhead box (FOX) family of transcription factors, is involved in mammalian development, physiology, and pathobiology. It has emerged as a key regulator of epithelial-to-mesenchymal transition (EMT) and tumour metastasis in cancers, especially digestive tract carcinomas. FOXQ1 may regulate gene expression by recruiting the MLL/KMT2 histone methyltransferase complex [2].

In pancreatic cancer, FOXQ1 overexpression promotes aerobic glycolysis, cell proliferation, tumour stemness, invasion, and metastasis by enhancing LDHA transcription [1]. In breast cancer, FOXQ1 recruits the MLL complex to activate EMT-related gene transcription and promote metastasis [2]. In ovarian cancer, FOXQ1 promotes cancer progression by activating the LAMB3/WNT/β-catenin signalling pathway [3]. In hepatocellular carcinoma, phosphorylated FOXQ1 inhibits sorafenib-induced ferroptosis by activating ETHE1 [4]. In breast cancer, FOXQ1 inhibits ferroptosis and tumour progression via the circ_0000643/miR-153/SLC7A11 axis [5]. In osteoarthritis, FOXQ1 inhibits disease progression by regulating pyroptosis [6].

In summary, Foxq1 is crucial in various biological processes and diseases. In cancer, it often promotes tumour-related phenotypes such as metastasis, proliferation, and resistance to treatment. In non-cancer conditions like sepsis-induced acute kidney injury, acute lung injury, and osteoarthritis, it has diverse roles in inflammation, apoptosis, and cell survival regulation. The study of Foxq1 in different genetic models helps understand its function in these biological processes and disease conditions, potentially guiding the development of new therapeutic strategies.