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7,8‐Dihydroxy‐4‐methylcoumarin induces apoptosis of human lung adenocarcinoma cells by ROS‐independent mitochondrial pathway through partial inhibition of ERK/MAPK signaling
Author(s) -
Goel Anita,
Prasad Ashok K.,
Parmar Virinder S.,
Ghosh Balaram,
Saini Neeru
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.04.052
Subject(s) - apoptosis , mapk/erk pathway , reactive oxygen species , a549 cell , downregulation and upregulation , mitochondrion , microbiology and biotechnology , signal transduction , chemistry , cancer research , biology , biochemistry , gene
Coumarins have attracted intense interest in recent years because they have been identified from natural sources, especially green plants and have diverse pharmacological properties. In this study, we investigated whether 7,8‐dihydroxy‐4‐methylcoumarin (DHMC) caused apoptosis in A549 human non‐small cell lung carcinoma cells (NSCLC) and, if so, by what mechanisms. Here, we show that, in A549 human NSCLC cells, DHMC induces apoptosis through mitochondria‐mediated caspase‐dependent pathway. Although an increase in the levels of reactive oxygen species (ROS) was observed, pre‐treatment with antioxidant showed no protective effect against DHMC‐induced apoptosis. In addition, our immunoblot data revealed that DHMC treatment led to down‐regulation of Bcl‐xl, Bax, p21, Cox‐2, p53 and upregulation of c‐Myc. Results in the present study for the first time suggest that DHMC induces apoptosis in human lung A549 cells through partial inhibition of ERK/MAPK signaling.