Astaxanthin Induces Apoptosis in MCF-7 Cells through a p53-Dependent Pathway.
MCF-7
apoptosis
astaxanthin
breast cancer
p53
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
28 Jun 2024
28 Jun 2024
Historique:
received:
06
06
2024
revised:
27
06
2024
accepted:
27
06
2024
medline:
13
7
2024
pubmed:
13
7
2024
entrez:
13
7
2024
Statut:
epublish
Résumé
Astaxanthin (3,3'-dihydroxy-β,β-carotene-4,4'-dione; AXT) is a xanthophyll β-carotenoid found in microalgae, seafood, fungi, complex plants, flamingos, and quail. It is well known that AXT plays a role as a drug with antioxidant and antitumor properties. Furthermore, several studies have reported that the reagent shows anti-inflammatory and neuroprotective effects. Recently, it was found that AXT acts as a peroxisome proliferator-activated receptor γ (PPARγ) modulator. To investigate the effect of AXT on MCF-7 cells (a human breast cancer cell line), the cells were treated with various concentrations of AXT. The treatment induced the decrease in cell number in a dose-dependent manner. Additionally, the Annexin V-positive cells were increased by the AXT treatment. These results indicated that apoptosis was induced in the tumor cells through the treatment of AXT. To elucidate the connection between apoptosis and p53, the levels of p53 and p21 proteins were assessed. Consequently, it was observed that the expression of p53 and p21 increased proportionally to the concentration of the AXT treatment. These findings suggest that the apoptosis of MCF-7 cells induced by AXT operates through a p53-dependent pathway, implying that AXT could potentially have a beneficial role in future breast cancer treatments. Thus, our results will provide a direction for future cancer challenges.
Identifiants
pubmed: 39000216
pii: ijms25137111
doi: 10.3390/ijms25137111
pii:
doi:
Substances chimiques
astaxanthine
8XPW32PR7I
Tumor Suppressor Protein p53
0
Xanthophylls
0
TP53 protein, human
0
Cyclin-Dependent Kinase Inhibitor p21
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : National Research Foundation of Korea
ID : NRF-2022R1I1A1A01053007