CANTHARIDIN INHIBITS COLON CANCER THROUGH miR-192-5p UPREGULATION

Abstract: Colon cancer (CC) is a serious threat to human health. Cantharidin (CTD) has anti-cancer properties. This study aims to explore the mechanism of CTD in treating CC. We used CCK-8, Transwell, and Annexin V/PI double staining analyses to detect the effects of CTD on the proliferation, migration, invasion, and apoptosis of CC cells. The effect of CTD on tumor growth was investigated by constructing a CC mouse model. Wild-type or mutant WNK1 luciferase vectors were constructed to verify the interaction between miR-192-5p and WNK1 mRNA. In the CTD group: miR-192-5p level was elevated and the OD values at 450 nm were significantly decreased; the quantity of CC cells passing the Transwell chamber (without or with matrigel) was reduced; the number of apoptotic cells increased obviously; the volume and weight of tumor decreased significantly. These results were reversed by miR-192-5p inhibitor. In HT-29 cells transfected with the wild-type WNK1 vector, the luciferase activity decreased with the miR-192-5p mimic but increased with the miR-192-5p inhibitor. The inhibitor of miR-192-5p counteracted the suppression of CTD on WNK1 expression. In summary, we demonstrated that CTD inhibited CC development by up-regulating miR-192-5p targeting WNK1, which will provide a theoretical basis for the application of CTD in the CC treatment.