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

作     者：Ashok Mari Gopikrishnan Mani Sirpu Natesh Nagabhishek Gopaiakrishnan Balaraman Nirmala Subramanian Fathima Bushra Mirza Jagan Sundaram Devaki Thiruvengadam Ashok Mari;Gopikrishnan Mani;Sirpu Natesh Nagabhishek;Gopalakrishnan Balaraman;Nirmala Subramanian;Fathima Bushra Mirza;Jagan Sundaram;Devaki Thiruvengadam

作者机构：Department of BiochemistryUniversity of MadrasGuindy CampusChennai(600025)India Cancer Biology LabDepartment of Nanoscience and NanotechnologySathyabama Institute of Science and TechnologyChennai(600119)India VRR Institute of Biomedical ScienceKattupakkamChennai(600056)India 

出 版 物：《Chinese Journal of Integrative Medicine》 (中国结合医学杂志（英文版）)

年 卷 期：2021年第27卷第9期

页      面：680-687页

核心收录：

学科分类：1008[医学-中药学(可授医学、理学学位)] 1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 1005[医学-中医学] 1002[医学-临床医学] 100602[医学-中西医结合临床] 10[医学] 

基　　金：support in the form of Senior Research Fellowship (SRF) 

主　　题：carvacrol breast cancer proliferation apoptosis PI3K/AKT signaling pathway 

摘      要：Objective:To examine the role of carvacrol in modulating PI3 K/AKT signaling involved in human breast cancer pathogenesis using in vitro experimental model MCF-7 ***:MTT and lactate dehydrogenase assays were performed with cells treated with different doses of carvacrol(0–250μmol/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 *** like cell cycle arrest and apoptosis were observed by flow cytometric analysis and expressions of p-Rb,cyclin D1,cyclin-dependent kinase 4(CDK4),CDK6,Bax,Bcl-2,PI3 K/p-AKT were analyzed by ***:Carvacrol significantly reduced cell viability with the half maximal inhibitory concentration value of 200μmol/L at 24 and 48 h(P0.05).importantly,there was a significant increase in the accumulation of the G0/G1 phase upon treatment with carvacrol in MCF-7 cells(P0.05 or P0.01).A remarkable decrease in protein expressions of p-Rb,cyclin D1,CDK4 and CDK6 denoted cell cycle arrest(P0.05 or P0.01).In addition,carvacrol treatment significantly inhibited PI3 K/p-AKT protein expressions leading to induction of apoptosis mediated by decreased Bcl2 and increased Bax protein ***,Annexin V/PI staining by FACS analysis,dual staining by AO/EB and PI staining studies suggested induction of apoptosis by carvacrol through PI3 K/Akt signaling pathway in MCF-7 ***:Carvacrol significantly inhibited the breast cancer MCF-7 cell proliferation and induced apoptosis via suppressing PI3/AKT signaling pathway.