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. 2018 Nov 13;9:1297. doi: 10.3389/fphar.2018.01297

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Copyright © 2018 Li, Liu, Yang, Xu, Lv, Zhang, Liu, Zhang and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic illustration showing the precise mechanism of myristoyl-CM4 in breast cancer. N-myristoylation significantly increased the membrane affinity toward breast cancer cells and also effectively mediated cellular entry. sialic acid-containing oligosaccharides (including O-mucin and gangliosides) were important targets for myristoyl-CM4 binding to breast cancer cells. After internalization, myristoyl-CM4 targeted mitochondria and induced mitochondrial dysfunction, including alterations in mitochondrial transmembrane potential, reactive oxygen species (ROS) generation and cytochrome c release. And then to activate caspase 9, caspase 3 and cleavage of PARP to induce mitochondria-dependent apoptosis in breast cancer cells.