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. 2016 Aug 24;7(41):67129–67141. doi: 10.18632/oncotarget.11562

Figure 7. Model of H2-18 as an effective antibody conquering trastuzumab resistance by inducing programmed cell death.

Figure 7

A. In trastuzumab-resistant breast cancer cells, trastuzumab plus pertuzumab is unable to effectively suppress cell growth both in vitro and in vivo due to sustained activated PI3K/AKT signaling caused by PI3K mutation or PTEN loss in these cells. B. In trastuzumab-resistant breast cancer cells, H2-18 also fails to suppress the aberrant activated PI3K/AKT signaling caused by PI3K mutation or PTEN loss. However, H2-18 can overcome trastuzumab resistance in vivo possibly due to its potent ability to induce cell death. H2-18 treatment can activate RIP1, resulting in ROS production and then activation of the pro-necrotic effect of JNK, ultimately leading to programmed necrosis.