Pumilio RNA binding family member 1 deficiency activates anti-tumor immunity in hepatocellular carcinoma via restraining M2 macrophage polarization

Abstract

Abstract Pumilio RNA binding family member 1 (PUM1), which has been implicated in both the progression of colorectal cancer and the regulation of Inflammation, has not yet been associated with hepatocellular carcinoma PUM1 is essential for the transition of tumor-associated macrophages (TAMs) into the M2 polarization state. It does this by inhibiting anti-tumor immunity in hepatocellular carcinoma through a process mediated by TAMs that target CD8 + T cells, as demonstrated in this study using PUM1-knockout mice. By activating the cAMP signaling pathway, we have shown that PUM1 promotes the transformation of TAMs into pro-tumorigenic M2-like phenotypes. In order to emphasize the potential of PUM1 as an objective for immunotherapy centered on TAMs in the treatment of gastric carcinoma, the present investigation revealed the molecular mechanism underlying the pro-tumor role of PUM1 in this cancer.