The antiproliferative potential and mechanism of action of metformin in MCF-7 cells.
antiproliferative
apoptosis
autophagy
breast cancer
metformin
Journal
Future science OA
ISSN: 2056-5623
Titre abrégé: Future Sci OA
Pays: England
ID NLM: 101665030
Informations de publication
Date de publication:
Jun 2023
Jun 2023
Historique:
received:
04
12
2022
accepted:
03
03
2023
pubmed:
14
5
2023
medline:
14
5
2023
entrez:
14
5
2023
Statut:
epublish
Résumé
The current study aimed to investigate the potential antiproliferative activity of metformin, the effective concentration range, and the mechanism of action. Human breast cancer cells, MCF-7 were treated with a serial dilution of metformin (10-150 μM) for 24 and 48 h. Potential antiproliferative activity of metformin and its ability in inducing cellular apoptosis and autophagy were also investigated. Metformin inhibited MCF-7 proliferation in a concentration and time dependent manner, with 80 μM as the most effective concentration. Compared with nontreated cells, metformin induced significant levels of autophagy and apoptosis, which were confirmed by the reduction of mTOR and BCL-2 protein expression. The study confirms the antiproliferative activity of metformin, which may likely occur through AMPK signaling pathway. The antidiabetic drug, metformin is tested in this work for its possible ability to inhibit the growth of breast cancer cells. Using different concentrations of the drug over different time points, the results showed that the drug was able to inhibit cancer growth through different mechanisms. The results also showed that the drug inhibits cancer growth by stimulating program cell death (apoptosis), as well as autophagy, where the cell breaks old and abnormal cellular substances.
Autres résumés
Type: plain-language-summary
(eng)
The antidiabetic drug, metformin is tested in this work for its possible ability to inhibit the growth of breast cancer cells. Using different concentrations of the drug over different time points, the results showed that the drug was able to inhibit cancer growth through different mechanisms. The results also showed that the drug inhibits cancer growth by stimulating program cell death (apoptosis), as well as autophagy, where the cell breaks old and abnormal cellular substances.
Identifiants
pubmed: 37180606
doi: 10.2144/fsoa-2022-0080
pmc: PMC10167719
doi:
Types de publication
Journal Article
Langues
eng
Pagination
FSO859Informations de copyright
© 2023 The Authors.
Déclaration de conflit d'intérêts
The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.