The effect of sulindac on redox homeostasis and apoptosis-related proteins in melanotic and amelanotic cells.
Apoptosis Regulatory Proteins
/ metabolism
Melanoma
/ metabolism
Sulindac
/ chemistry
Homeostasis
/ drug effects
Oxidation-Reduction
Humans
Cell Line, Tumor
Antioxidants
/ pharmacology
Superoxide Dismutase
/ metabolism
Glutathione Peroxidase
/ metabolism
Catalase
/ metabolism
Hydrogen Peroxide
/ metabolism
Signal Transduction
/ drug effects
Amelanotic melanoma
Cancer
Dacarbazine
Melanotic melanoma
Sulindac
p53/Bax/Bcl-2 proteins
Journal
Pharmacological reports : PR
ISSN: 2299-5684
Titre abrégé: Pharmacol Rep
Pays: Switzerland
ID NLM: 101234999
Informations de publication
Date de publication:
Aug 2023
Aug 2023
Historique:
received:
27
01
2023
accepted:
05
05
2023
revised:
04
05
2023
medline:
28
7
2023
pubmed:
17
5
2023
entrez:
17
5
2023
Statut:
ppublish
Résumé
Non-steroidal anti-inflammatory drugs have been shown to inhibit the development of induced neoplasms. Our previous research demonstrated that the cytotoxicity of sulindac against melanoma cells is comparable to dacarbazine, the drug used in chemotherapy. The aim of this study was to investigate the mechanism of sulindac cytotoxicity on COLO 829 and C32 cell lines. The influence of sundilac on the activity of selected enzymes of the antioxidant system (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)) and the content of hydrogen peroxide as well as the level of proteins initiating (p53, Bax) and inhibiting (Bcl-2) apoptosis were measured in melanoma cells. In melanotic melanoma cells, sulindac increased the activity of SOD and the content of H The cytotoxic effect of sulindac in the COLO 829 cell line is connected to disturbed redox homeostasis by changing the activity of SOD, CAT, GPx, and level of H
Sections du résumé
BACKGROUND
BACKGROUND
Non-steroidal anti-inflammatory drugs have been shown to inhibit the development of induced neoplasms. Our previous research demonstrated that the cytotoxicity of sulindac against melanoma cells is comparable to dacarbazine, the drug used in chemotherapy. The aim of this study was to investigate the mechanism of sulindac cytotoxicity on COLO 829 and C32 cell lines.
METHODS
METHODS
The influence of sundilac on the activity of selected enzymes of the antioxidant system (superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)) and the content of hydrogen peroxide as well as the level of proteins initiating (p53, Bax) and inhibiting (Bcl-2) apoptosis were measured in melanoma cells.
RESULTS
RESULTS
In melanotic melanoma cells, sulindac increased the activity of SOD and the content of H
CONCLUSION
CONCLUSIONS
The cytotoxic effect of sulindac in the COLO 829 cell line is connected to disturbed redox homeostasis by changing the activity of SOD, CAT, GPx, and level of H
Identifiants
pubmed: 37195561
doi: 10.1007/s43440-023-00493-1
pii: 10.1007/s43440-023-00493-1
pmc: PMC10374796
doi:
Substances chimiques
Apoptosis Regulatory Proteins
0
Sulindac
184SNS8VUH
Antioxidants
0
Superoxide Dismutase
EC 1.15.1.1
Glutathione Peroxidase
EC 1.11.1.9
Catalase
EC 1.11.1.6
Hydrogen Peroxide
BBX060AN9V
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
995-1004Subventions
Organisme : Śląski Uniwersytet Medyczny w Katowicach
ID : PCN-1-013/K/2/F
Informations de copyright
© 2023. The Author(s).
Références
J Cell Biochem. 2022 Jun;123(6):1077-1090
pubmed: 35535453
Carcinogenesis. 2008 Feb;29(2):390-7
pubmed: 18174252
Am J Surg. 1989 Jan;157(1):175-9
pubmed: 2535920
J Exp Clin Cancer Res. 2000 Mar;19(1):21-34
pubmed: 10840932
Vet Res Commun. 2014 Mar;38(1):29-38
pubmed: 24126842
Oncogene. 2008 Apr 17;27(18):2648-55
pubmed: 18059344
ISRN Dermatol. 2013 Apr 11;2013:616170
pubmed: 23691346
Postepy Hig Med Dosw (Online). 2006;60:439-46
pubmed: 17013363
Lancet Oncol. 2009 May;10(5):501-7
pubmed: 19410194
Anal Biochem. 1973 Apr;52(2):517-21
pubmed: 4698846
Med Sci Monit. 2005 Jan;11(1):BR22-9
pubmed: 15614186
Mol Pharm. 2022 Dec 5;19(12):4487-4505
pubmed: 36305753
Profiles Drug Subst Excip Relat Methodol. 2016;41:323-77
pubmed: 26940170
J Biol Chem. 1951 Nov;193(1):265-75
pubmed: 14907713
Acta Dermatovenerol Croat. 2014;22(1):1-12
pubmed: 24813835
Cancer Biol Ther. 2007 Jan;6(1):30-9
pubmed: 17172818
Neoplasia. 2007 Mar;9(3):192-9
pubmed: 17401459
J Surg Oncol. 1983 Sep;24(1):83-7
pubmed: 6887943
Pharmacol Res. 2020 Feb;152:104499
pubmed: 31689521
Apoptosis. 2007 Jan;12(1):195-209
pubmed: 17136320
Environ Toxicol Pharmacol. 2013 Nov;36(3):769-78
pubmed: 23958969
J Invest Dermatol. 2001 Aug;117(2):333-40
pubmed: 11511312
Pharmaceuticals (Basel). 2010 May 25;3(5):1652-1667
pubmed: 27713322
Cancers (Basel). 2021 Sep 30;13(19):
pubmed: 34638397
J Am Acad Dermatol. 2000 May;42(5 Pt 1):731-4
pubmed: 10775846
PLoS One. 2015 Mar 05;10(3):e0118702
pubmed: 25742310
Postepy Hig Med Dosw (Online). 2011 Nov 23;65:734-51
pubmed: 22173438
Clin Pharmacokinet. 1997 Jun;32(6):437-59
pubmed: 9195115
Cancer. 2012 Dec 1;118(23):5848-56
pubmed: 22605570
Eur J Pharmacol. 2008 Mar 31;583(1):26-31
pubmed: 18291362
Sci Rep. 2016 Jan 18;6:19534
pubmed: 26777116
Cancer Lett. 1983 Nov;21(1):57-61
pubmed: 6640513
Ginekol Pol. 2011 Mar;82(3):195-9
pubmed: 21735687