Myristoyl-modified BMAP-28m affects the cell cycle and apoptosis of prostate cancer cells by damaging the cell membrane

myr-BMAP-28m targeting of prostate cancer was developed by us in this study, to reveal the efficacy and principle of myr-BMAP-28m and compare BMAP-28m. It was found that compared with BMAP-28m, myr-BMAP-28m showed stronger cytotoxicity against prostate cancer cells than normal cells, thus yielding good tumor cell-targeting effect. Mechanistic study demonstrated that myr-BMAP-28m could arrest prostate cancer cells at the G1 phase, then induce apoptosis for prostate cancer cells with highly increased expression levels of apoptosis proteins. Its mode of action involves being attached to the cancer cell membrane, forming pores and penetrating into the cells, which results in an increase in lactate dehydrogenase (LDH) released from cells.Experiments including JC-1 staining, reactive oxygen species (ROS) detection, RHO123 staining, adenosine triphosphate (ATP) measurement, and scanning electron microscopy observation confirmed that myr-BMAP-28m could induce mitochondrial damage in cancer cells. In vivo experimental results showed that myr-BMAP-28m effectively inhibited the growth of prostate tumors with minimal adverse effects on host mice. Further verification via immunohistochemistry (IHC) assays indicated that after treatment with myr-BMAP-28m, the expression of apoptosis-related proteins was upregulated, while the expression of proliferation-related proteins was downregulated in tumor tissues. This study provides experimental evidence for the development of myr-BMAP-28m as a candidate drug for prostate cancer therapy.