Mechanistic studies have revealed that Pt-1 exerts its antitumor effects through dual pathways: on the one hand, it upregulates the pro-apoptotic protein caspase-3 (15.24% vs. 7.3%) and downregulates the anti-apoptotic protein Bcl-2 (10.9% vs. 19.7%), thereby inducing apoptosis from both aspects; on the other hand, it downregulates the expression of the cell proliferation marker Ki-67 (2.25% vs. 4.95%), thus inhibiting the proliferation of tumor cells. This evidence concerns the gene BCL2 and neoplasm.