Coptisine induces apoptosis in non-small cell lung cancer NCI-H1650 cells through ROS-dependent mito-chondria pathway
YANG Fan
LI Xin
ZHANG Tingting
LI Jianrong
ZHU Yihua
HU Yahui
LIU Hua
Abstract：Objective To explore the effect of coptisine on the growth of NCI-H1650cells and to evaluate its potential value in the treatment of human non-small cell lung cancer. Methods MTT method was used to ana-lyze cell proliferation. Protein expressions of Bax/Bcl-2 and cytochrome C in NCI-H1650 cells were detected by-Western blot.Apoptosis was analyzed using flow cytometrywithAnnexin V/PI method.ROS concentration was tested with fluorometry.Results Coptisine could significantly inhibit growth of NCI-H1650 cells in a time-and dose-de-pendent manner.Coptisine induced apoptosis in NCI-H1650 cells by inducing ROS accumulation and the following mitochondria mediated apoptosis which was identified by increased Bax expression,Bcl-2 expression was down-reg-ulated,and cytochrome C moved from mitochondria to cytoplasm.ROS inhibitor(N-acetyl cysteine)treatment dra-matically abrogated coptisine-induced growth inhibition and apoptosis.Conclusions This study suggests that copti-sine can induce ROS irritated-and mitochondria-mediated apoptosis in NCI-H1650 cells.Coptisine has a potential value in the treatment of human non-small cell lung cancer.
Keywords：coptisineapoptosisROSnon-small cell lung cancerNCI-H1650 cells
Publication Date：2017-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 4033-4037 )