Oxidative stress and antioxidants in the pathophysiology of malignant melanoma
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Elena Obrador
, Feng Liu-Smith , Ryan W. Dellinger , Rosario Salvador , Frank L. Meyskens und José M. Estrela
Abstract
The high number of somatic mutations in the melanoma genome associated with cumulative ultra violet (UV) exposure has rendered it one of the most difficult of cancers to treat. With new treatment approaches based on targeted and immune therapies, drug resistance has appeared as a consistent problem. Redox biology, including reactive oxygen and nitrogen species (ROS and RNS), plays a central role in all aspects of melanoma pathophysiology, from initiation to progression and to metastatic cells. The involvement of melanin production and UV radiation in ROS/RNS generation has rendered the melanocytic lineage a unique system for studying redox biology. Overall, an elevated oxidative status has been associated with melanoma, thus much effort has been expended to prevent or treat melanoma using antioxidants which are expected to counteract oxidative stress. The consequence of this redox-rebalance seems to be two-fold: on the one hand, cells may behave less aggressively or even undergo apoptosis; on the other hand, cells may survive better after being disseminated into the circulating system or after drug treatment, thus resulting in metastasis promotion or further drug resistance. In this review we summarize the current understanding of redox signaling in melanoma at cellular and systemic levels and discuss the experimental and potential clinic use of antioxidants and new epigenetic redox modifiers.
Funding: Ministerio de Economia, Industria y Competitividad (Spain), Grant Number: SAF2017-83458-R.
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©2019 Walter de Gruyter GmbH, Berlin/Boston
Artikel in diesem Heft
- Frontmatter
- Reviews
- Complexity of type IV collagens: from network assembly to function
- Structural and mechanistic aspects of S-S bonds in the thioredoxin-like family of proteins
- Oxidative stress and antioxidants in the pathophysiology of malignant melanoma
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Dynamic characteristics of the mitochondrial genome in SCNT pigs
- Protein Structure and Function
- Conversion of chenodeoxycholic acid to cholic acid by human CYP8B1
- Molecular Medicine
- The comparative biochemistry of viruses and humans: an evolutionary path towards autoimmunity
- MiR-23a-3p-regulated abnormal acetylation of FOXP3 induces regulatory T cell function defect in Graves’ disease
- Cell Biology and Signaling
- Evidence for a protective role of the CX3CL1/CX3CR1 axis in a model of amyotrophic lateral sclerosis
- LncRNA TINCR/microRNA-107/CD36 regulates cell proliferation and apoptosis in colorectal cancer via PPAR signaling pathway based on bioinformatics analysis
- Regulatory effect of hsa-miR-5590-3P on TGFβ signaling through targeting of TGFβ-R1, TGFβ-R2, SMAD3 and SMAD4 transcripts
Artikel in diesem Heft
- Frontmatter
- Reviews
- Complexity of type IV collagens: from network assembly to function
- Structural and mechanistic aspects of S-S bonds in the thioredoxin-like family of proteins
- Oxidative stress and antioxidants in the pathophysiology of malignant melanoma
- Research Articles/Short Communications
- Genes and Nucleic Acids
- Dynamic characteristics of the mitochondrial genome in SCNT pigs
- Protein Structure and Function
- Conversion of chenodeoxycholic acid to cholic acid by human CYP8B1
- Molecular Medicine
- The comparative biochemistry of viruses and humans: an evolutionary path towards autoimmunity
- MiR-23a-3p-regulated abnormal acetylation of FOXP3 induces regulatory T cell function defect in Graves’ disease
- Cell Biology and Signaling
- Evidence for a protective role of the CX3CL1/CX3CR1 axis in a model of amyotrophic lateral sclerosis
- LncRNA TINCR/microRNA-107/CD36 regulates cell proliferation and apoptosis in colorectal cancer via PPAR signaling pathway based on bioinformatics analysis
- Regulatory effect of hsa-miR-5590-3P on TGFβ signaling through targeting of TGFβ-R1, TGFβ-R2, SMAD3 and SMAD4 transcripts