Premium
Signaling pathway for aloe‐emodin‐induced apoptosis in human H460 lung nonsmall carcinoma cell
Author(s) -
Yeh FengTsgh,
Wu ChunHsiung,
Lee HongZin
Publication year - 2003
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.11185
Subject(s) - emodin , aloe emodin , apoptosis , programmed cell death , protein kinase a , p38 mitogen activated protein kinases , biology , kinase , signal transduction , microbiology and biotechnology , cell culture , cancer research , chemistry , biochemistry , genetics
Aloe‐emodin (1,8‐dihydroxy‐3‐(hydroxymethyl)‐anthraquinone) is an active component from the root and rhizome of Rheum palmatum that has been reported to exhibit antitumor effects through an unknown mechanism. Our study investigated the mechanisms of aloe‐emodin‐induced cell death in the human lung nonsmall cell carcinoma cell line H460. Aloe‐emodin (40 μM)‐induced apoptosis of H460 cells involves modulation of cAMP‐dependent protein kinase, protein kinase C, Bcl‐2, caspase‐3 and p38 protein expression. The relationship of various signals involved in cell death, such as cAMP‐dependent protein kinase, protein kinase C, Bcl‐2, caspase‐3 and p38, has been investigated in the regulation of apoptotic cell death of aloe‐emodin. We demonstrated that the expression of p38 is an important determinant of apoptotic death induced by aloe‐emodin. © 2003 Wiley‐Liss, Inc.