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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: HSPA4 upregulation induces immune evasion via ALKBH5/CD58 axis in gastric cancer

Fig. 6

HSPA4/ALKBH5/CD58 axis in patients with GC. A Representative pictures of mfIHC for HSPA4, ALKBH5, CD58 and CD8 in GC patients’ specimens. Cell nuclei were counterstained with DAPI (scale bar=50 µm). B The survival curve showed that HSPA4 upregulation correlated with poor five-year survival with GC patients. C The average fluorescence intensity of ALKBH5, CD58 and CD8 in tumor tissues with different HSPA4 expression levels were summarized. D The correlation between average fluorescence intensity of ALKBH5 and HSPA4 (left), as well as ALKBH5 and CD58 (right) in tumor tissues were analyzed by Pearson’s correlation. E The correlation between average fluorescence intensity of HSPA4 and average density of CD8+ T cell (left), as well as fluorescence intensity of HSPA4 and distance from CD8+ T cells to ALKBH5+HSPA4+ cells (right) were analyzed by Pearson’s correlation. F Representative pictures of mfIHC for HSPA4, ALKBH5 and CD58 in GC patients receiving PD1 blockade therapy (SYSUCC). Cell nuclei were counterstained with DAPI (scale bar=50 µm). G Box plots with the expression of HSPA4, ALKBH5 and CD58 from responders and non-responders of PD1 blockade therapy (SYSUCC) (Wilcoxon rank-sum test). H Box plots showed the RNA levels of HSPA4, ALKBH5 and CD58 from responders and non-responders of PD1 blockade therapy (SRA data (https://ncbi.nlm.nih.gov/sra) analyzed by TIGER) (Wilcoxon rank-sum test). (*, P<0.05; **, P<0.01; ***, P<0.001)

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