CTNNB1 and colonic neoplasm: To evaluate this hypothesis, we performed loss-of-function studies in HCT116 cells, which is derived from a microsatellite instable human colon tumor with mutations in CTNNB1, KRAS, and TGFBR3. Specifically, we treated HCT116 cells with a miR-24-3p locked nucleic acid (LNA) inhibitor, which led to significantly reduced detection of miR-24-3p (Fig. 5A).