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. This evidence concerns the gene CASP3 and colorectal carcinoma.