Yes.
PD-1 is a receptor protein (located outside the cell) expressed on T-cells (a type of lymphocyte - an immune cell). A PD-1 inhibitor is known as an immune checkpoint inhibitor that binds to PD-1 on a T-cell. When a PD-1 inhibitor binds to PD-1 on T-cells it enables the T-cell to kill tumor cells. IFN-g (a cell killing cytokine) expression is increased in PD-1 therapies (among many other likely molecular changes, but relevant to the story of FTO and the paper above). This can be sumarised as PD-1 inhibitors activate T-cells and increase expression of IFN-g.
Based on the article I posted above, FTO inhibitors selectively bind and inhibit FTO (inside the cell) decreasing the production of the genes PD-1, CXCR4, and SOX10, which leads to a reduction in cancer cell number, migration, invasion, and cell viability. Also, FTO inhibition sensitizes melanoma cells (makes them vulnerable) to IFN-g (a molecule upregulated by PD-1 therapies), which aids in cancer cell death. This can be sumarised as FTO inhibitors influence the production of genes within the cell which influences multiple protumorigenic factors and sensitizes melanoma cells to a molecule expressed in PD-1 therapies, IFN-g.
I know more about FTO inhibitors than PD-1 therapies, but there's my best effort. Let me know if this makes sense.
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