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. 2023 Jan 21;24(2):130–145. doi: 10.1007/s11864-023-01053-8

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Dynamic roles of autophagy in melanoma. (1) Schematic representation of autophagy process. (2) BRAFi induces transcriptional activation of autophagy-lysosome program (by disrupting ERK-mediated TFEB phosphorylation and promoting p38-MAPK-mediated phosphorylation/inactivation of the autophagy repressor ZKSCAN3) and its blockade causes tumor progression, metastasis, and drug resistance that is associated with enhanced TGF-β signaling. (3) CQ modes of action in addition to inhibition of autophagy flux. This includes but not limited to TFEB activation and nuclear translocation (in part, by pH-dependent calcium release through MCOLN1), p38 and NF-κB signaling activation (following calcium release) and consequent macrophage polarization (from M2 to M1) and associated increased anti-tumor immunity, telomeric G-quadruplex binding, PUMA stabilization and induced apoptosis, as well as ISR activation (through eIF2α phosphorylation). MEK, mitogen-activated protein kinase; ERK, extracellular signal-regulated kinase; p38-MAPK, mitogen-activated protein kinase; TFEB, transcription factor EB; ZKSCAN3, zinc finger with KRAB and SCAN domains; CQ/HCQ, chloroquine/hydroxychloroquine; MCOLN1, Mucolipin-1; PPT1, Palmitoyl-protein thioesterase 1; NF-κB, nuclear factor kappa B; MDSCs, myeloid-derived suppressor cells; Tregs, regulatory T cells; ISR, integrated stress response; PUMA, p53 upregulated modulator of apoptosis. This figure was created with BioRender.com.