• KLF7 is overexpressed in cervical cancer tissues and correlates with poor patient survival, acting as an oncogene.
• KLF7 promotes cervical cancer cell proliferation, migration, invasion, and metabolic reprogramming by modulating key genes like PFKL and ACADL.
• Knockout of KLF7 Exon 2 paradoxically increases nuclear KLF7 and oncogenic potential, highlighting complex regulatory mechanisms.
• Alpha-lipoic acid (ALA) downregulates KLF7 expression and suppresses cervical cancer progression, suggesting a potential therapeutic strategy.