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Kruppel-like factor 17 (KLF17) is a member of the Krüppel-like family of transcription factors, which are characterized by three conserved C-terminal C2H2-type zinc finger motifs that enable sequence-specific DNA binding[2][4][1]. KLF17 primarily regulates gene expression and has a critical role in controlling cell proliferation, differentiation, and the inhibition of epithelial-mesenchymal transition (EMT), functioning as a tumor suppressor in several cancers[3]. In addition to its key roles in cancer biology, KLF17 is essential for physiological processes such as spiral artery remodeling during pregnancy via transcriptional activation of targets like CORIN[5]. KLF17 is typically located in the nucleus, and its dysregulation or suppression—often due to promoter methylation—can contribute to tumor progression and metastasis[3]. KLF17 is also classified as a zinc finger transcription factor based on structure and function, and it is not currently a direct therapeutic target with known small-molecule or biologic drugs[3]. Notes: - KLF17 is not considered a classical drug target such as a receptor, enzyme, or transporter, but is significant as a transcriptional regulator implicated in disease pathogenesis, especially as a tumor suppressor[3][4]. - No drugs are documented to directly target KLF17; it is studied as a biomarker and in experimental modulation for cancer and pregnancy disorders[3][5].
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