Krueppel-like factor 5 (KLF5)

Krueppel-like factor 5 (KLF5) is a zinc finger transcription factor predominantly expressed in proliferating epithelial cells and is a key regulator of cell proliferation, differentiation, migration, apoptosis, and stemness[1][2][3][4]. KLF5 binds GC box motifs in gene promoters and directly regulates transcription in response to multiple signaling pathways including Ras/MAPK, PKC, TGFβ, and retinoic acid pathways, with its expression and activity tightly regulated by complex posttranslational modifications such as phosphorylation, acetylation, ubiquitination, and sumoylation[1]. KLF5’s function is context-dependent, able to promote or suppress cell proliferation, and its dysregulation is widely implicated in the pathogenesis of cancer and cardiovascular diseases, making it both a potential diagnostic biomarker and a therapeutic target[1][4]. Drugs that modulate KLF5 function, particularly targeted inhibitors and retinoid derivatives, are under study for their effects on cell cycle and proliferation, although disruptions to KLF5 activity can also present therapeutic challenges due to its essential roles in normal tissue homeostasis and regeneration[1][4].

Other names

BTEB2Basic transcription element binding protein 2Colon Krueppel-like factorIntestinal-enriched Krueppel-like factorGC-box-binding protein 2Transcription factor BTEB2CKLFIKLFEpididymis secretory sperm binding protein

Retinoic acid and derivatives inhibit KLF5 transcription and function via receptor-mediated signaling.\nPI3K and RTK inhibitors suppress KLF5 transcription, affecting downstream proliferation and differentiation pathways.