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. 2022 Dec 9;4(4):zcac038. doi: 10.1093/narcan/zcac038

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© The Author(s) 2022. Published by Oxford University Press on behalf of NAR Cancer.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — Inhibiting Prmt1 or Ripk1 downregulates expression levels of genes associated with poor clinical responses to adoptive T cell transfer (ACT). (A) Enrichment plots of gene sets associated with ACT responses in tumor samples with gene-specific perturbations. The mRNA expression profiles of tumor cell lines derived from pre-treatment tumor tissues in ACT-treated melanoma patients were previously determined. Based on clinical response to ACT (RECIST v.1.1), patients were stratified into the non-responders (with stable or progressive disease) and responders (with complete or partial response) groups. Differentially expressed genes (P< 0.05, by two-sided t-test) between tumor cells from non-responders and responders were identified. Upregulated genes and downregulated genes in non-responders were defined as the ‘ACT-Non-responder’ set and the ‘ACT-Responder’ set, respectively. Results from the control group in the in vitro-CROP screen were used to determine whether these two target sets are differentially expressed between MC38/GC cells with or without gene-specific-KO (gRNA versus gNC). NES, normalized enrichment score; FDR, false discovery rate. The value of FDR ≤0.25 was recognized as the statistical significance and labeled with red color. (B) A Venn diagram showing the number and list of overlapped and unique genes that are from the ACT-non-responder set and differentially expressed in gPrmt1 or gRipk1 cells. (C) Heatmaps demonstrating the relative expression levels of selected ACT-non-responder genes in melanoma lines derived from pre-treated tumor tissues. Genes that are differentially expressed in gPrmt1 or gRipk1 cells were selected for illustration.