Figure 3.

Various hnRNP-mediated molecular mechanisms regulate cancer-immune crosstalk. HnRNP increase tumor proliferation, migration, metastasis, metabolic deregulation, and therapeutic resistance. In myeloid cells, hnRNP can induce cell differentiation, polarization, expansion, infiltration, or act either as activators or repressors of the immune response. HnRNP in cancer cells regulate the production of chemokines that recruit myeloid cells into the TME. On the other hand, in myeloid cells, hnRNP control the generation of immunosuppressive or inflammatory cytokines to fuel uncontrolled tumor growth and metastasis. HnRNP-mediated effects in cancer and myeloid cells create a crosstalk, promoting a pro-tumor landscape.