Krüppel-like factor (KLF) family is highly conserved zinc finger transcription factors that regulate cell proliferation, differentiation, apoptosis, and migration. KLF17 is a member of the KLF family. Recent studies have demonstrated that KLF17 low expression and inactivation are caused by microRNA, gene mutation, and loss of heterozygosity in human tumors, which participates in tumor progression. KLF17 low expression increases cancer metastatic viability; its mechanism is that low KLF17 mediates epithelial-mesenchymal transition (EMT) through regulating EMT-related genes expression; the reduced-KLF17 also increases cancer metastasis though upregulating inhibitor of DNA binding 1 (ID1). Additionally, mutant p53 proteins are capable of developing a complex with KLF17, which mediate the depletion of KLF17 inhibiting EMT gene transcription and increases cancer metastasis. KLF17 downregulation also mediates the activation of TGF-β pathway.