Fig. 2
From: Melanoma biology and treatment: a review of novel regulated cell death-based approaches
Pyroptosis and its role in melanoma. Pyroptosis can be activated by four pathways: (1) the canonical pathway with inflammasome assembly and caspase-1 activation (2) the noncanonical pathway with caspase-4/5/11 activation by direct binding of its N-terminal CARD domain to intracellular LPS. (3) Caspase 3/8-mediated pathway with GSDMC or GSDME cleavage (4) Granzyme-mediated pathway with granzyme A and B, secreted from cytotoxic T lymphocytes and NK cells respectively, can cleave GSDMB and GSDME, respectively. Research of pyroptosis on melanoma was expressed in white squares with reference number in parenthesis. The exogenous molecules are marked in blue squares especially. GSDME cleavage by activated caspase 3 has been observed by chemotherapeutic drugs, BRAF and MEK inhibitors/ PDPK1 and MEK inhibitors, and ROS production with iron dextran or raptinal, a caspase 3 activator. Caspase-1 DNA was ever included in anticancer DNA vaccine to induce pyroptosis of melanoma cells. Pyroptosis can also be induced by temozolomide and chloroquine via autophagy inhibition and inflammasome activation