ChloroquineV1, Main, Exploration, bibRecord, 001544

Lysosomal membrane permeabilization is involved in curcumin-induced apoptosis of A549 lung carcinoma cells

Identifieur interne : 001544 ( Main/Exploration ); précédent : 001543; suivant : 001545

Lysosomal membrane permeabilization is involved in curcumin-induced apoptosis of A549 lung carcinoma cells

Auteurs : Qing-Yong Chen [République populaire de Chine] ; Jian-Guo Shi [République populaire de Chine] ; Qing-Hua Yao [République populaire de Chine] ; De-Min Jiao [République populaire de Chine] ; Yan-Yi Wang [République populaire de Chine] ; Hui-Zhen Hu [République populaire de Chine] ; Yu-Quan Wu [République populaire de Chine] ; Jia Song [République populaire de Chine] ; Jie Yan [République populaire de Chine] ; Li-Jun Wu [République populaire de Chine]

Source :

Molecular and Cellular Biochemistry [ 0300-8177 ] ; 2012-01-01.

RBID : ISTEX:9B44DEC530BA5B4144B916F877A6A6851E260C50

English descriptors

KwdEn :
- Apoptosis, Curcumin, Lung cancer, Lysosomal membrane permeabilization, Reactive oxygen species.

Abstract

Abstract: We previously reported that curcumin inhibited lung cancer A549 cells growth and promoted cell apoptosis in vitro. In this study, we further examined the apoptosis-related parameters, including lysosomal damage and cathepsin activation, in A549 cells exposed to curcumin. We found that curcumin caused lysosomal membrane permeabilization (LMP) and cytosolic relocation of cathepsin B (cath B) and cathepsin D (cath D). However, only Z-FA-fmk (a cath B inhibitor) but not pepstatin A (a cath D inhibitor) inhibited curcumin-induced cell apoptosis, mitochondrial membrane potential loss, and cytochrome c release. The antioxidant N-acetylcysteine and glutathione attenuated LMP, suggesting that lysosomal destabilization was dependent on the elevation of reactive oxygen species and which precedes mitochondrial dysfunction. These findings indicated a novel pathway for curcumin regulation of ROS-lysosomal–mitochondrial pathway and provided the key mechanism of regulation of LMP in cell apoptosis, which may be exploited for cancer treatment.

Url:

https://api.istex.fr/ark:/67375/VQC-MHMD7580-T/fulltext.pdf

DOI: 10.1007/s11010-011-1033-9

Affiliations:

République populaire de Chine

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Le document en format XML

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<front><div type="abstract" xml:lang="en">Abstract: We previously reported that curcumin inhibited lung cancer A549 cells growth and promoted cell apoptosis in vitro. In this study, we further examined the apoptosis-related parameters, including lysosomal damage and cathepsin activation, in A549 cells exposed to curcumin. We found that curcumin caused lysosomal membrane permeabilization (LMP) and cytosolic relocation of cathepsin B (cath B) and cathepsin D (cath D). However, only Z-FA-fmk (a cath B inhibitor) but not pepstatin A (a cath D inhibitor) inhibited curcumin-induced cell apoptosis, mitochondrial membrane potential loss, and cytochrome c release. The antioxidant N-acetylcysteine and glutathione attenuated LMP, suggesting that lysosomal destabilization was dependent on the elevation of reactive oxygen species and which precedes mitochondrial dysfunction. These findings indicated a novel pathway for curcumin regulation of ROS-lysosomal–mitochondrial pathway and provided the key mechanism of regulation of LMP in cell apoptosis, which may be exploited for cancer treatment.</div>
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Lysosomal membrane permeabilization is involved in curcumin-induced apoptosis of A549 lung carcinoma cells

Lysosomal membrane permeabilization is involved in curcumin-induced apoptosis of A549 lung carcinoma cells

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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