Carvacrol Promotes Cell Cycle Arrest and Apoptosis through PI3K/AKT Signaling Pathway in MCF-7 Breast Cancer Cells.

Autor: Mari A; Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India., Mani G; Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India., Nagabhishek SN; Cancer Biology Lab, Department of Nanoscience and Nanotechnology, Sathyabama Institute of Science and Technology, Chennai, 600119, India., Balaraman G; Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India., Subramanian N; Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India., Mirza FB; VRR Institute of Biomedical Science, Kattupakkam, Chennai, 600056, India., Sundaram J; Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India., Thiruvengadam D; Department of Biochemistry, University of Madras, Guindy Campus, Chennai, 600025, India. devakit@yahoo.co.uk.
Jazyk: angličtina
Zdroj: Chinese journal of integrative medicine [Chin J Integr Med] 2021 Sep; Vol. 27 (9), pp. 680-687. Date of Electronic Publication: 2020 Jun 22.
DOI: 10.1007/s11655-020-3193-5
Abstrakt: 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 0 /G 1 phase upon treatment with carvacrol in MCF-7 cells (P<0.05 or P<0.01). A remarkable decrease in protein expressions of p-Rb, cyclin D1, CDK4 and CDK6 denotes cell cycle arrest (P<0.05 or P<0.01). In addition, carvacrol treatment significantly inhibited PI3K/p-AKT protein expressions leading to induction of apoptosis mediated by decreased Bcl2 and increased Bax protein expressions. Further, Annexin V/PI staining by FACS analysis, dual staining by AO/EB and PI staining studies suggests induction of apoptosis by carvacrol through PI3K/Akt signaling pathway in MCF-7 cells.
Conclusion: Carvacrol significantly inhibited the breast cancer MCF-7 cell proliferation and induced apoptosis via suppressing PI3/AKT signaling pathway.
(© 2020. The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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