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Effects of redox modulation on quiescin/sulfhydryl oxidase activity of melanoma cells.
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- Author(s): Mazepa E;Mazepa E; Furlanetto ALDM; Furlanetto ALDM; Brum H; Brum H; Nakao LS; Nakao LS; Martinez PA; Martinez PA; Cadena SMSC; Cadena SMSC; Rocha MEM; Rocha MEM; Cunha ES; Cunha ES; Martinez GR; Martinez GR
- Source:
Molecular and cellular biochemistry [Mol Cell Biochem] 2024 Mar; Vol. 479 (3), pp. 511-524. Date of Electronic Publication: 2023 Apr 27.- Publication Type:
Journal Article- Language:
English - Source:
- Additional Information
- Source: Publisher: Springer Country of Publication: Netherlands NLM ID: 0364456 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1573-4919 (Electronic) Linking ISSN: 03008177 NLM ISO Abbreviation: Mol Cell Biochem Subsets: MEDLINE
- Publication Information: Publication: New York : Springer
Original Publication: The Hague, Dr. W. Junk B. V. Publishers. - Subject Terms:
- Abstract: Secreted quiescin/sulfhydryl oxidase (QSOX) is overexpressed in many tumor cell lines, including melanoma, and is usually associated with a pro-invasive phenotype. Our previous work described that B16-F10 cells enter in a quiescent state as a protective mechanism against damage generated by reactive oxygen species (ROS) during melanogenesis stimulation. Our present results show that QSOX activity was two-fold higher in cells with stimulated melanogenesis when compared to control cells. Considering that glutathione (GSH) is one of the main factor responsible for controlling redox homeostasis in cells, this work also aimed to investigate the relationship between QSOX activity, GSH levels and melanogenesis stimulation in B16-F10 murine melanoma cell line. The redox homeostasis was impaired by treating cells with GSH in excess or depleting its intracellular levels through BSO treatment. Interestingly, GSH-depleted cells without stimulation of melanogenesis kept high levels of viability, suggesting a possible adaptive mechanism of survival even under low GSH levels. They also showed lower extracellular activity of QSOX, and higher QSOX intracellular immunostaining, suggesting that this enzyme was less excreted from cells and corroborating with a diminished extracellular QSOX activity. On the other hand, cells under melanogenesis stimulation showed a lower GSH/GSSG ratio (8:1) in comparison with control (non-stimulated) cells (20:1), indicating a pro-oxidative state after stimulation. This was accompanied by decreased cell viability after GSH-depletion, no alterations in QSOX extracellular activity, but higher QSOX nucleic immunostaining. We suggest that melanogenesis stimulation and redox impairment caused by GSH-depletion enhanced the oxidative stress in these cells, contributing to additional alterations of its metabolic adaptive response.
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Ganig N, Baenke F, Thepkaysone M-L, Lin K, Rao VS, Wong FC, Polster H, Schneider M, Helm D, Pecqueux M, Seifert AM, Seifert L, Weitz J, Rahbari NN, Kahlert C (2021) Proteomic analyses of fibroblast- and serum-derived exosomes identify QSOX1 as a marker for non-invasive detection of colorectal cancer. Cancers 13:1351–1380. https://doi.org/10.3390/cancers130613510. (PMID: 10.3390/cancers130613510338027648002505) - Grant Information: 88887.372486/2019-00 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior; 422547/2018-3 Conselho Nacional de Desenvolvimento Científico e Tecnológico
- Contributed Indexing: Keywords: Glutathione; Melanogenesis; Melanoma; QSOX; Redox
- Accession Number: GAN16C9B8O (Glutathione)
EC 1.- (Oxidoreductases)
0 (Reactive Oxygen Species)
EC 1.8.3.- (sulfhydryl oxidase)
EC 1.8.3.2 (QSOX1 protein, mouse)
EC 1.8.- (Oxidoreductases Acting on Sulfur Group Donors) - Publication Date: Date Created: 20230427 Date Completed: 20240325 Latest Revision: 20240404
- Publication Date: 20240404
- Accession Number: 10.1007/s11010-023-04745-9
- Accession Number: 37103678
- Source:
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