Targeting autophagy as a potential therapeutic approach for melanoma therapy

• Published in: Seminars in cancer biology Vol. 23; no. 5; pp. 352 - 360
• Main Authors: Liu, He, He, Zhaoyue, Simon, Hans-Uwe
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-10-2013
• Subjects: Animals; Autophagy; Autophagy - drug effects; Chemotherapy; Hematology, Oncology and Palliative Medicine; Humans; Hypoxia; Immunotherapy; Melanoma; Melanoma - drug therapy; Melanoma - metabolism; Melanoma - pathology; Signal Transduction; Cav-1; DNA damage response; endophilin B1; MHC; DN; major histocompatibility complex; progression free survival; Bif-1; PEDF; PI3P; PI3K; Immunotherapy; autophagy-related; LAMP2; mTOR; phophatidylinositol-3-phosphate; DRiPs; PFS; LC3; dysplastic nevi; TRAIL; cytotoxic T-lymphocyte antigen 4; human leukocyte antigen; Melanoma; EM; radial growth phase; ER; defective ribosomal products; caveolin-1; vertical growth phase; Chemotherapy; ROS; PCL; Hypoxia; RGP; ULK1; bafilomycin A1; HLA; phosphoinositide 3-kinase; VGP; 3-methyladenine; antigen-presenting cell; pigment epithelium-derived factor receptor; tissue microarray; AMBRA1; ganoderic acid-dextromethorphan; BN; Autophagy; chloroquine; IFN; microtubule-associated protein 1 light chain 3; UV radiation resistance associated gene; mammalian target of rapamycin; benign nevi; DDR; lysosomal-associated membrane protein 2; skin-derived precursor; reactive oxygen species; electron microscopy; tumor necrosis factor-related apoptosis-inducing ligand; CTLA-4; GA-DM; polyethylene imine; 5-ALA; unc-51-like kinase 1; ASS; UVRAG; HIF; cytolytic T lymphocyte; TMA; hypoxia-inducible factor; polygonatum cyrtonema lectin; autophagy/Beclin 1 regulator 1; interferon; CQ; argininosuccinate synthetase; phosphatidylethanolamine; APC; ATG; PE; PEI; Ataxia telangiectasia mutated; BafA1; 3-MA; SKP; ATM; CTL; 5-aminolevulinic acid; endoplasmic reticulum
• ISSN: 1044-579X; 1096-3650
• DOI: 10.1016/j.semcancer.2013.06.008

Abstract Melanoma, occurring as a rapidly progressive skin cancer, is resistant to current chemo- and radiotherapy, especially after metastases to distant organs has taken place. Most chemotherapeutic drugs exert their cytotoxic effect by inducing apoptosis, which, however, is often deficient in cancer cells. Thus, it is appropriate to attempt the targeting of alternative pathways, which regulate cellular viability. Recent studies of autophagy, a well-conserved cellular catabolic process, promise to improve the therapeutic outcome in melanoma patients. Although a dual role for autophagy in cancer therapy has been reported, both protecting against and promoting cell death, the potential for using autophagy in cancer therapy seems to be promising. Here, we review the recent literature on the role of autophagy in melanoma with respect to the expression of autophagic markers, the involvement of autophagy in chemo- and immunotherapy, as well as the role of autophagy in hypoxia and altered metabolic pathways employed for melanoma therapy.