Hypoxia Modulates Melanoma Cells Proliferation and Apoptosis via miRNA-210/ISCU/ROS Signaling

Suwei, D.; Lei, Zhen; Zhimin, L.; Mei, Liyan; Jianping, K.; Zhuohui, P.; Yanbin, X.; Xiang, Mengqin

doi:10.1007/s10517-022-05605-0

Cited by 2 publications

(1 citation statement)

References 12 publications

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“…Hypoxic stress can cause the overproduction of reactive oxygen species, which can inhibit the activity of antioxidant enzymes such as thioredoxin reductase 1 [50]. Suvei et al [51] reported that CoCl 2 -induced hypoxia decreased the viability of human melanoma cells (A2058 and G361), increased ROS production, and induced cell apoptosis. Reduction in thioredoxin reductase 1 of both mRNA and protein levels was observed in EM56 and DT cells [50].…”

Section: Discussionmentioning

confidence: 99%

Hypoxia-Induced Changes in L-Cysteine Metabolism and Antioxidative Processes in Melanoma Cells

Rydz,

Wróbel,

Janik

et al. 2023

Biomolecules

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This study was performed on human primary (WM115) and metastatic (WM266-4) melanoma cell lines developed from the same individual. The expression of proteins involved in L-cysteine metabolism (sulfurtransferases, and cystathionine β-synthase) and antioxidative processes (thioredoxin, thioredoxin reductase-1, glutathione peroxidase, superoxide dismutase 1) as well as the level of sufane sulfur, and cell proliferation under hypoxic conditions were investigated. Hypoxia in WM115 and WM266-4 cells was confirmed by induced expression of carbonic anhydrase IX and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 by the RT-PCR and Western blot methods. It was shown that, under hypoxic conditions the inhibition of WM115 and WM266-4 melanoma cell proliferation was associated with decreased expression of thioredoxin reductase-1 and cystathionine β-synthase. These two enzymes may be important therapeutic targets in the treatment of melanoma. Interestingly, it was also found that in normoxia the expression and activity of 3-mercaptopyruvate sulfurtransferase in metastatic WM266-4 melanoma cells was significantly higher than in primary melanoma WM115 cells.

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Section: Discussionmentioning

confidence: 99%

Hypoxia-Induced Changes in L-Cysteine Metabolism and Antioxidative Processes in Melanoma Cells

Rydz,

Wróbel,

Janik

et al. 2023

Biomolecules

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Epigenetics and Control of Tumor Angiogenesis in Melanoma: An Update with Therapeutic Implications

Cazzato,

Sgarro,

Casatta

et al. 2024

Cancers

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Angiogenesis, the formation of new blood vessels from pre-existing ones, is a crucial process in the progression and metastasis of melanoma. Recent research has highlighted the significant role of epigenetic modifications in regulating angiogenesis. This review comprehensively examines the current understanding of how epigenetic mechanisms, including DNA methylation, histone modifications, and non-coding RNAs, influence angiogenic pathways in melanoma. DNA methylation, a key epigenetic modification, can silence angiogenesis inhibitors such as thrombospondin-1 and TIMP3 while promoting pro-angiogenic factors like vascular endothelial growth factor (VEGF). Histone modifications, including methylation and acetylation, also play a pivotal role in regulating the expression of angiogenesis-related genes. For instance, the acetylation of histones H3 and H4 is associated with the upregulation of pro-angiogenic genes, whereas histone methylation patterns can either enhance or repress angiogenic signals, depending on the specific histone mark and context. Non-coding RNAs, particularly microRNAs (miRNAs) further modulate angiogenesis. miRNAs, such as miR-210, have been identified as key regulators, with miR-9 promoting angiogenesis by targeting E-cadherin and enhancing the expression of VEGF. This review also discusses the therapeutic potential of targeting epigenetic modifications to inhibit angiogenesis in melanoma. Epigenetic drugs, such as DNA methyltransferase inhibitors (e.g., 5-azacytidine) and histone deacetylase inhibitors (e.g., Vorinostat), have shown promise in preclinical models by reactivating angiogenesis inhibitors and downregulating pro-angiogenic factors. Moreover, the modulation of miRNAs and lncRNAs presents a novel approach for anti-angiogenic therapy.

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Hypoxia Modulates Melanoma Cells Proliferation and Apoptosis via miRNA-210/ISCU/ROS Signaling

Cited by 2 publications

References 12 publications

Hypoxia-Induced Changes in L-Cysteine Metabolism and Antioxidative Processes in Melanoma Cells

Hypoxia-Induced Changes in L-Cysteine Metabolism and Antioxidative Processes in Melanoma Cells

Epigenetics and Control of Tumor Angiogenesis in Melanoma: An Update with Therapeutic Implications

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