Mechanistically, the interaction site between KLF3 and WNT1 promoter leads to an upregulation in WNT1 transcription, thereby inducing stimulation of the WNT/β-catenin axis; in contrast, when WNT1 is inhibited, it mitigates the proliferative, migratory, and invasive capacity of CRC cells induced by suppressed KLF3 expression. Here, KLF3 is linked to colorectal carcinoma.