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. 2024 Jun 29;15:5502. doi: 10.1038/s41467-024-49673-4

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© The Author(s) 2024, corrected publication 2025

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — a Workflow of identification of potential targets against oxaliplatin resistance using druggable gene CRISPR knockout screens. b Venn diagram of preferably druggable gene hits (ΔSLC43A2^OR-1, ΔTP53^OR-2 or ΔCDKN1A^OR-1 vs. Vector; HCT116^OR, HCT8^OR, DLD1^OR vs. corresponding untreated Mock) in six oxaliplatin-resistant cell lines. c The RRA scores of all the tested genes for oxaliplatin-sensitive control or -resistance cells in each comparison. The genes in red box are preferential targets against resistance. d The prominently enriched functional terms for druggable gene sets against oxaliplatin in six resistant cell lines. Unpaired two-sided t test for p value with Benjamini-Hochberg (BH) adjustment. e Immunoblot analysis validating the knockout effect of PLK4 or PLK1. sgCtrl, empty control sgRNA vector. f Cell growth effect of PLK4 knockout in oxaliplatin-sensitive or -resistant cell lines. Mean ± SD with n = 3 biological replicates. Unpaired two-sided t test (ΔSLC43A2^OR, ΔTP53^OR or ΔCDKN1A^OR vs. sgAAVS1; HCT116^OR vs. Mock) for p value. g Expression of PLK4-WT but not kinase-dead mutant PLK4-D154A rescues the growth inhibition caused by PLK4 knockout in oxaliplatin-resistant cells. Mean ± SD with n = 3 biological replicates. Unpaired two-sided t test for p value. h–j Cell growth inhibition by two independent sgRNAs targeting PLK4 in oxaliplatin-resistant DLD1 (h), HCT8 (i) and HT29 (j) cells. Mean ± SD with n = 3 biological replicates. Unpaired two-sided t test for p value. k Cell growth effect of indicated cell lines treated with DMSO or 12 nM CFI-400945 for 7 days. Mean ± SD with n = 3 biological replicates. Unpaired two-sided t test (ΔSLC43A2^OR, ΔTP53^OR or ΔCDKN1A^OR vs. sgAAVS1; HCT116^OR vs. Mock) for p value. l–n Cell growth inhibition of DLD1 (l), HCT8 (m) and HT29 (n) cells by 10 nM CFI-400945 for 11 days, 15 nM CFI-400945 for 11 days, and 15 nM CFI-400945 for 10 days, respectively. Mean ± SD with n = 3 biological replicates. Unpaired two-sided t test for p value.