Carvacrol Promotes Cell Cycle Arrest and Apoptosis through PI3K/AKT Signaling Pathway in MCF-7 Breast Cancer Cells.
10.1007/s11655-020-3193-5
- Author:
Ashok MARI
1
;
Gopikrishnan MANI
1
;
Sirpu Natesh NAGABHISHEK
2
;
Gopalakrishnan BALARAMAN
1
;
Nirmala SUBRAMANIAN
1
;
Fathima Bushra MIRZA
3
;
Jagan SUNDARAM
1
;
Devaki THIRUVENGADAM
4
Author Information
1. Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India.
2. Cancer Biology Lab, Department of Nanoscience and Nanotechnology, Sathyabama Institute of Science and Technology, Chennai, 600119, India.
3. VRR Institute of Biomedical Science, Kattupakkam, Chennai, 600056, India.
4. Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India. devakit@yahoo.co.uk.
- Publication Type:Journal Article
- Keywords:
PI3K/AKT signaling pathway;
apoptosis;
breast cancer;
carvacrol;
proliferation
- From:
Chinese journal of integrative medicine
2021;27(9):680-687
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To examine the role of carvacrol in modulating PI3K/AKT signaling involved in human breast cancer pathogenesis using in vitro experimental model MCF-7 cells.
METHODS:MTT and lactate dehydrogenase assays were performed with cells treated with different doses of carvacrol (0-250 p mol/L) at different time points (24 and 48 h). The nuclear morphology was assessed in MCF-7 cells with propidium iodide (PI) and acridine orange/ethidium bromide (AO/EB) staining and analyzed by fluorescence microscopy. Events like cell cycle arrest, apoptosis was observed by flow cytometric analysis and expressions of p-Rb, cyclin D1, cyclin-dependent kinase 4 (CDK4), CDK6, Bax, Bcl-2, PI3K/p-AKT was analyzed by immunoblot.
RESULTS:Carvacrol significantly reduced cell viability with the half maximal inhibitory concentration value of 200 µmol/L at 24 and 48 h (P<0.05). importantly, there was a significant increase in the accumulation of the G
CONCLUSION:Carvacrol significantly inhibited the breast cancer MCF-7 cell proliferation and induced apoptosis via suppressing PI3/AKT signaling pathway.