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. 2022 Sep 26;13:1007429. doi: 10.3389/fphar.2022.1007429

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Copyright © 2022 He, Liang, Huang, Jiang, Liu, Sun, Li, Cong and Jiang.

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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Combined treatment of GEM and IKE synergistically inhibited the proliferation of A549 and PC9. (A) A549 cell viability was assessed by CCK8 assay after treatment with different concentrations of GEM alone (0, 10, 50, 100 or 200 nM) or in combination with IKE (2 or 5 μM) for 48 h (B) PC9 cell viability was assessed by CCK8 assay after treatment with different concentrations of GEM alone (0, 100, 500, 1000 or 2000 nM) or in combination with IKE (2 or 5 μM) for 48 h (C,D) The software calculated and evaluated the combination index (CI) of GEM and IKE in A549 and PC9. CI = 1, additive; CI > 1, antagonism; CI < 1, synergism. (E) Venn diagram showing ferroptosis driver genes upregulated by GEM treatment in A549. (F) Venn diagram showing ferroptosis suppressors downregulated by GEM treatment in A549. n = 3. GEM: Gemcitabine; IKE: Imidazole Ketone Erastin; CCK8 assay: Cell Counting Kit-8 assay; CI: combination index.