Foxk2, short for Forkhead box K2, is a central transcriptional regulator in embryonic development and cell homeostasis. As a member of the forkhead box transcription factor family, it contains a conserved winged-helix DNA-binding domain. Foxk2 mediates various biological processes such as genomic stability, DNA repair, cell proliferation, apoptosis, and cell metabolism. It is involved in pathways like nucleotide de novo synthesis and aerobic glycolysis, and its dysregulation is linked to cancer development [1,2,3,4].

In breast cancer, knockdown of Foxk2 significantly inhibited cell proliferation, migration, and anchorage-independent growth, and delayed tumor growth in a xenograft mouse model, suggesting its oncogenic role in this context [5]. In multiple myeloma, silencing Foxk2 by siRNA prevented the expression of PFKFB3 via dephosphorylation of AMP-activated protein kinase, inhibiting glycolysis and cell proliferation [6]. In hepatocellular carcinoma, Foxk2 directly regulates nucleotide synthetic genes, promoting tumor growth and cancer cell resistance to chemotherapy [7].

In conclusion, Foxk2 is a crucial transcription factor involved in multiple biological processes. Through gene-knockout or conditional-knockout mouse models and other loss-of-function experiments, its role in cancer development and progression has been revealed, especially in breast cancer, multiple myeloma, and hepatocellular carcinoma. Understanding Foxk2's functions may provide potential therapeutic targets for these diseases.