Fig. 7: Immune checkpoint blockade (ICB) disrupted the HDAC2-AS2-CDK9 axis to empower CDK9+ CD8+ T cell cytotoxicity. | Nature Communications

Fig. 7: Immune checkpoint blockade (ICB) disrupted the HDAC2-AS2-CDK9 axis to empower CDK9+ CD8+ T cell cytotoxicity.

From: HBV-associated hepatocellular carcinomas inhibit antitumor CD8+ T cell via the long noncoding RNA HDAC2-AS2

Fig. 7

a The scRNA-seq (GEO: GSE151530 and GSE149614) UMAP projection of the tumor-infiltrating T cells from patients with liver cancer. Each color represents a T-cell cluster. Cell types and marker genes are assigned to each cluster. b UMAP plot showing the information of patients with or without immune checkpoint blockade (ICB) therapy. c Violin plot showing the expression profiles of indicated genes. These T-cell groups were grouped based on the ICB therapy and expression of CD4, CD8A, and CDK9 in each cell. A Wilcoxon Rank Sum test was performed to determine the P values (two-tailed test). d Experimental layout to analyze the effect of anti-PD-1treatment in inhibiting tumor growth in C57BL/6 WT mice (n = 7 mice). Mice were subcutaneously xenografted with Hepa1-6-Ctrl or HDAC2-AS2 cells (1 × 107) for 16 days and received anti-PD-1 treatment at day 7 and day 9. e and f Tumor volumes (e) and Tumor weight (f) are shown in C57BL/6 WT mice subcutaneously xenografted with Hepa1-6-Ctrl or HDAC2-AS2 cells and received anti-PD-1 treatment. n = 7. g The disease-free survival curve based on the TCGA HCC data showing patients with higher expression of CDK9 and CD8A, or CDK9 and HDAC2-AS2 in tumor had better prognosis. Log-rank test was performed to determine the P values. h Working model. Error bars represent mean ± SEM. Statistical analyses were determined by two-way ANOVA (e) or two-tailed Student’s t-test (f). Source data are provided as a Source Data file.

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