Fig. 2

DUSP1 is indispensable for minimal residual disease and CD4⁺ T cell cytotoxity. A Significant ligand-receptor pairs of cell communication between T cells, which were grouped as DUSP1⁺ and DUSP1⁻, with other cell types. B UMAP embedding overlaid with unsupervised cluster cell type annotations of T cells integrating seven datasets. C DUSP1 expression in pre- and post-chemotherapy patient sample in CD4⁺ T_CTL cell (left) and CD4⁺ T_TSG cell (right). *p < 0.05. D UMAP embedding overlaid with unsupervised cluster cell type annotations of fibroblast cells integrating seven datasets. E DUSP1 expression in pre- and post-chemotherapy patient sample in inflammatory CAF cell (left) and vascular CAF cell (right). *p < 0.05. F Volcano plot showing the gene profile change between persister and control cells of RNA seq results. The red dots represent the genes that are significantly up-regulated in persister cells, and the blue dots represent the genes that are significantly down-regulated in persister cells. G Western blot showing DUSP1 expression in persister cells of three different cell line. H Microscopic images of human cancer cells treated with Torin1 plus chemotherapeutic agents (10 nM paclitaxel). The images are representative of three biological replicates. The average cell count per image is indicated in the lower right corner. Scale bar, 100 μm. The column blot shows the number of persister. *p < 0.05. I Tumor growth of mouse subcutaneous xenograft model using control or DUSP1 KO cells treated or not with chemotherapeutics. The minimal residual disease and relapase time line is shown across groups. *p < 0.05. J Survival of mice bearing wild type and DUSP1 knockout tumors with or without chemotherapeutics treatment for 4 weeks. *p < 0.05. K GSEA results using the canonical pathway gene sets in DUSP1 KO vs wild type pair. Normalized enrichment scores (NES). L, M. Flow cytometry was used to analyze the proportion and cytotoxicity of CD4⁺ T cells in the DUSP1 KO and wild type cells. *p < 0.05