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. 2020 Oct 27;8:597835. doi: 10.3389/fcell.2020.597835

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Copyright © 2020 Shimizu, Fujii and Sakai.

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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The molecular mechanism of the cisplatin resistance in human epidermoid carcinoma cells. In the cisplatin-sensitive KB cells, cisplatin induces F-actin polymerization, enhancing the activation of the VSOR anion channels and K⁺ channels. Their activation results in sustained cell shrinkage, apoptotic volume decrease (AVD), leading to apoptosis. On the other hand, the cisplatin-resistant KCP-4 cells exhibit the disruption of F-actins. The deficiency of F-actin rearrangement after cisplatin treatment attenuates the activation of the VSOR anion channels, causing the cisplatin resistance. KCP-4 cells treated with trichostatin A (TSA) shows clear F-actins, recovering the VSOR anion channel activities and its cisplatin sensitivity.