Fig. 1
From: Melanoma biology and treatment: a review of novel regulated cell death-based approaches
Schematic diagram of autophagy-dependent cell death and related research in melanoma. Autophagy is a process initiated by ULK1 complex formation, followed by membrane isolation and phagospore formation. After fusion with lysosome, autophagosome ends up and engulfed substrates are digested in autophagosome. Related researches are expressed in white squares with reference number in parenthesis. The exogenous small molecules are marked in blue squares especially. For example, vemurafenib (a BRAF inhibitor) resistance is associated with elevated expression of Beclin-1, ATG5 and UVRAG, and its efficacy can be increased by ectopic expression of miR-216b to inhibit ATG5. The manipulation of autophagy can also influence the immune response in melanoma, such as increased local infiltration of NK cells in melanoma after inhibition of Beclin-1, ATG5 or p62 correlated with increased expression of CCL5 and improved prognosis. Loss of BNIP3 decreased macrophage phagocytosis of dying melanoma cells. Besides, autophagy activity is associated with MDSC- mediated suppression of anti-melanoma immunity, melanoma adaption to fluctuating O2 or pH, and outcome of targeted therapy with temozolomide and sorafenib