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Signaling pathway for aloe-emodin-induced apoptosis in human H460 lung nonsmall carcinoma cell

✍ Scribed by Feng-Tsgh Yeh; Chun-Hsiung Wu; Hong-Zin Lee


Book ID
102271468
Publisher
John Wiley and Sons
Year
2003
Tongue
French
Weight
295 KB
Volume
106
Category
Article
ISSN
0020-7136

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✦ Synopsis


Abstract

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.


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Aloe-emodin (1,8-dihydroxy-3-(hydroxymethyl)-anthraquinone) is one of the active constituents from the root and rhizome of Rheum palmatum. Our previous study has demonstrated that aloe-emodin induced a significant change in the expression of lung cancer cell apoptosis-related proteins compared to th