Figure 2.

Proposed model for the targeting of NRAS-mutant melanoma by ERβ ligands. In NRAS-mutant melanoma cells (BLM), ERβ agonists trigger genomic effects at the nuclear level by modulating the expression of cell cycle-related proteins and by reversing the global hypomethylation status of these cells. Moreover, it is hypothesized that activated ERβ might also exert non-genomic effects, by interfering with the PI3K/Akt signaling pathway, as previously described for different cancer cell lines expressing this receptor.