Fig. 7
From: HSPA4 upregulation induces immune evasion via ALKBH5/CD58 axis in gastric cancer
Proposed model depicting HSPA4 modulating immune evasion and response to PD1 blockade. HSPA4 is upregulated via promoter acetylation in GC tumor tissues. HSPA4 upregulation inhibits ALKBH5 degradation, leading to downregulation of CD58 in GC cells via m6A demethylation activity of ALKBH5, PDL1 upregulation in tumor cells and impairing cytotoxicity of CD8+ T cells, finally to immune evasion of tumor cells. Cytotoxicity of CD8+ T cells is re-activated in the presence of anti-PD1 checkpoint therapy