Kruppel-like factor 3 (KLF3)

Kruppel-like factor 3 (KLF3), also known as Basic Kruppel-like factor (BKLF), is a member of the zinc finger transcription factor family characterized by three C-terminal C2H2-type zinc fingers [5, 6]. It primarily functions as a transcriptional repressor by binding to CACCC boxes and GC-rich elements in gene promoters and recruiting co-repressors such as C-terminal binding protein (CtBP) [6, 11]. KLF3 plays critical roles in diverse biological processes, including erythropoiesis, B cell development, adipogenesis, and the regulation of inflammatory responses [2, 7, 11, 14]. In oncology, KLF3 exhibits context-dependent roles, acting as either a tumor suppressor or an oncogene depending on the cancer type; for instance, it is often downregulated in lung and colorectal cancers but may promote progression in others via the WNT/beta-catenin pathway [1, 2, 3, 15]. While no drugs specifically targeting KLF3 are currently approved, it is being investigated as a potential therapeutic target and prognostic biomarker, with research focusing on small molecule modulators and microRNA-mediated regulation [2, 8, 10]. Its broad involvement in metabolic and hematopoietic homeostasis presents both opportunities for multi-disease applications and challenges regarding systemic safety and specificity [6, 11, 14].

Other names

Basic Kruppel-like factorBKLFCACCC-box-binding protein BKLFTEF-2Kruppel-like factor 3 (basic)KLF transcription factor 3

KLF3 functions primarily as a transcriptional repressor by binding to CACCC-box and GC-rich DNA elements via its C-terminal zinc fingers and recruiting the C-terminal binding protein (CtBP) co-repressor complex [6, 11, 14]. It also modulates key oncogenic and developmental pathways, such as activating WNT1 to stimulate WNT/beta-catenin signaling in certain cancers or repressing STAT3 and Galectin-3 to regulate metastasis and inflammation [1, 3, 11, 15].