H. pylori-induced apoptosis in human gastric cancer cells mediated via the release of apoptosis-inducing factor from mitochondria.
H. pylori-induced apoptosis in human gastric cancer cells mediated via the release of apoptosis-inducing factor from mitochondria.
复制标题
DOI：
10.1111/j.1523-5378.2008.00646.x
复制
发表时间：
2008-12
期刊：
影响因子：
4.4
通讯作者：
Smoot DT
中科院分区：
文献类型：
--
作者：
Ashktorab H;Dashwood RH;Dashwood MM;Zaidi SI;Hewitt SM;Green WR;Lee EL;Daremipouran M;Nouraie M;Malekzadeh R;Smoot DT
Our previous study of H. pylori-induced apoptosis showed the involvement of Bcl-2 family proteins and cytochrome c release from mitochondria. Here, we examine the release of other factors from mitochondria, such as apoptosis inducing factor (AIF), and upstream events involving caspase-8 and Bid. Human gastric adenocarcinoma (AGS) cells were incubated with a cagA-positive H. pylori strain for 0, 3, 6 and 24 h and either total protein or cytoplasmic, nuclear and mitochondrial membrane fractions were collected. Proteins were immunoblotted for AIF, Bid, poly adenosine ribose polymerase (PARP), caspase-8 and β-catenin. H. pylori activated caspase-8, caused PARP cleavage, and attenuated mitochondrial membrane potential. A time-dependent decrease in β-catenin protein expression was detected in cytoplasmic and nuclear extracts, coupled with a decrease in β-actin. An increase in the cytoplasmic pool of AIF was seen as early as 3 h after H. pylori exposure, and a concomitant increase was seen in nuclear AIF levels up to 6 h. A band corresponding to full-length Bid was seen in both the cytoplasmic and nuclear fractions of controls, but not after H. pylori exposure. Active AIF staining was markedly increased in gastric mucosa from infected persons, compared to uninfected controls. H. pylori might trigger apoptosis in AGS cells via interaction with death receptors in the plasma membrane, leading to the cleavage of procaspase-8, release of cytochrome c and AIF from mitochondria, and activation of subsequent downstream apoptotic events, as reported previously for chlorophyllin. This is consistent with AIF activation that was found in the gastric mucosa of humans infected with H. pylori. Hence, the balance between apoptosis and proliferation in these cells may be altered in response to injury caused by H. pylori infection, leading to an increased risk of cancer.
登录
查看更多内容
影响因子：
5.8
作者：
Ahmed, A;Smoot, D;Ashktorab, H
通讯作者：
Ashktorab, H
影响因子：
64.8
作者：
Enari, M;Sakahira, H;Nagata, S
通讯作者：
Nagata, S
DOI：
10.1084/jem.187.10.1659
发表时间：
1998-05-18
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Fan X;Crowe SE;Behar S;Gunasena H;Ye G;Haeberle H;Van Houten N;Gourley WK;Ernst PB;Reyes VE
通讯作者：
Reyes VE
DOI：
10.1084/jem.187.4.487
发表时间：
1998-02-16
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Fan T;Lu H;Hu H;Shi L;McClarty GA;Nance DM;Greenberg AH;Zhong G
通讯作者：
Zhong G
影响因子：
6.4
作者：
HAGUE, A;MANNING, AM;PARASKEVA, C
通讯作者：
PARASKEVA, C