Survivin-3B (S-3B), an alternative splice isoform of survivin, plays a key role in tumorigenesis. S-3B promotes the escape of malignant cells from immune recognition by blocking the cytotoxicity of natural killer (NK) cells. Such an effect reflects the ability of S-3B to interfere with the assembly of the so-called "death-inducing signaling complex" upon the interaction of FAS with its ligand (FASL). S-3B also inhibits the activation of caspase-6, thus increasing the resistance of neoplastic cells to granzyme B and various chemotherapeutics.
Keywords: caspase-6; caspase-8; survivin-3B; treatment response; tumor escape; tumorigenesis.