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. 2016 Sep 20;18(9):525–535. doi: 10.1016/j.neo.2016.07.004

Figure 5.

Figure 5

(A) MTT analysis of wild-type and ATF3−/− MEFs following 48-hour treatments of cisplatin, carboplatin, doxorubicin, and docetaxel. Loss of ATF3 inhibits cisplatin-, carboplatin-, and doxorubicin-induced cytotoxicity but had no effect on docetaxel cytotoxicity. *Significant difference in the viability curves comparing the wild-type and the ATF3−/− MEFs responses (P< .05). (B) MTT analysis of Calu6, Calu6cisR1, H23, and H23cisR1 following 48-hour treatments with docetaxel showing no significant differences in sensitivity (note: cisplatin, carboplatin, and doxorubicin treatments were presented in Figure 1A). (C) Western blot analysis shows significant ATF3 induction restricted to the parental cell lines with cisplatin and carboplatin treatments. Doxorubicin treatments showed similar ATF3 induction in both the parental and their cisR1 sublines. No significant ATF3 induction was observed with the docetaxel treatments in any of the lines tested, with a weak induction in the H23 series (24-hour treatments, IC50 dose).