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. 2024 Aug 2;14(8):e1754. doi: 10.1002/ctm2.1754

FIGURE 1.

FIGURE 1

ABCC2‐24C > T polymorphism is associated with better clinical outcomes in gastric cancer patients. (A) The mutational landscape for the SNPs related to platinum/5‐Fu‐based chemotherapy resistance in this study. (B&C) Survival analysis of ABCC2 rs717620 and the wild type in cohort 1(left) and validation cohort (right). (D) Immunohistochemistry using DAB (brown), showing the expression of ABCC2 in gastric cancer tissues. Scale bar: 200 and 50 µm. Low (−/+), Moderate (++), High (+++). (E) Multi‐variate Cox regression analysis for assessment of the prognostic parameters of ABCC2 expression and different clinicopathological characteristics. (F) Kaplan‐Meier survival analysis of OS according to ABCC2 levels in 1022 GC patients for gastric cancer. (G, H) Kaplan‐Meier survival analysis of OS according to ABCC2 levels in the TCGA database and GSE84437 dataset. (I, J) The IHC (I) and mRNA (J) expression levels of ABCC2 in patients with the ABCC2‐24C > T genotype. *p < 0.05, ***p < 0.001; Student's t‐test. (K) CRISPR/Cas9 monoclonal screen to stably express the ABCC2 point mutation (24C > T) in the gastric cancer cell line SGC‐7901. The expression of ABCC2 was subsequently determined and quantified by western blot analysis. (L) Predicted transcription factors based on the ABCC2‐24C > T variant. (M) The dual luciferase assay showed SOX9 and ETS1 could significantly repress luciferase expression in the normal genotype. SGC‐7901 cells were cotransfected with either empty vector plasmid (Promoter‐NC), or the ABCC2 promoter plasmid (promoter‐NM/promoter‐SNP) and SOX9 or ETS1 expression plasmid.