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. 2020 Feb 3;10:46. doi: 10.3389/fonc.2020.00046

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Copyright © 2020 Wang, Lu, Dai, Fu, Hao, Zhao, Chen and Fu.

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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Knock-down of Met prevents the Cav-1-induced cisplatin resistance of AGS cells by targeting the Met and HER2 pathway. (A) The viability of AGS/Cav-1+ cells was elevated compared with AGS cells, while AGS/shMet cells were more sensitive to cisplatin than AGS/Cav-1+ cells. (B) Cav-1 stimulated the activation of Met, p-HER2 at Tyr1221/1222 site and total HER2 in AGS cells. Met silencing inhibited the increase of p-HER2 at Tyr1221/1222 site and total HER2 induced by Cav-1. (C) The relative levels of p-HER2 at Tyr1221/1222, total HER2 and Cav-1 in AGS cells were analyzed. (D) The fold change of p-HER2 relative to total HER2 in AGS cells was analyzed. *P < 0.05, **P < 0.01, ***P < 0.001 compared with control group. ^###P <0.001 compared with Cav-1 overexpression group. CDDP, cisplatin.