Astaxanthin Induces Apoptosis in MCF-7 Cells through a p53-Dependent Pathway.


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
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

Auteurs

Koanhoi Kim (K)

Department of Pharmacology, School of Medicine, Pusan National University, Busan 43241, Republic of Korea.

Hyok-Rae Cho (HR)

Department of Neurosurgery, College of Medicine, Kosin University, Busan 49267, Republic of Korea.

Yonghae Son (Y)

Department of Pharmacology, School of Medicine, Pusan National University, Busan 43241, Republic of Korea.

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Classifications MeSH