In our study, it is found that Wnt3 depletion also increased the cellular apoptosis via upregulating the expression of some proapoptotic genes, activating caspase 3 cleavages and an increase in PARP, enhanced the sensitivity of HCT-116 cells to cisplatin by facilitating caspase-dependent apoptosis, which is opposite to the result that overexpression of Wnt3 suppresses the apoptosis of CRC cells in the treatment of cisplatin. Here, WNT3 is linked to colorectal carcinoma.