内质网应激与肿瘤细胞的凋亡

被引：13

作者：

原玉芬

杨惠玲

机构：

[1] 中山大学中山医学院病理生理学教研室

来源：

分子诊断与治疗杂志 | 2010年 / 2卷 / 02期

关键词：

内质网应激; 未折叠蛋白反应; 肿瘤; 凋亡;

D O I：

暂无

中图分类号：

R730.2 [肿瘤病理学、病因学];

学科分类号：

100214 [肿瘤学];

摘要：

内质网(endoplasmic reticulum,ER)是重要的细胞器,是蛋白质合成、折叠、组装和钙离子储存等的场所。多种生理和病理条件下,如缺氧、氧化还原状态的改变等可干扰内质网的功能,并引起未折叠蛋白在ER中堆积,产生内质网应激(endoplasmic reticulum stress,ERS)。虽然ERS可诱导细胞的生存,然而长时间过强的ERS可诱导细胞凋亡,即内质网应激反应性凋亡。

引用

页码：128 / 134

页数：7

共 18 条

[1]

Endoplasmic reticulum stress mediates γ-tocotrienol-induced apoptosis in mammary tumor cells [J].

Wali, Vikram B. ;

Bachawal, Sunitha V. ;

Sylvester, Paul W. .

APOPTOSIS, 2009, 14 (11) :1366-1377

[2]

Oxidative and endoplasmic reticulum stress signaling are involved in dehydrocostuslactone-mediated apoptosis in human non-small cell lung cancer cells.[J].Jen-Yu Hung;Ya-Ling Hsu;Wen-Chiu Ni;Ying-Ming Tsai;Chih-Jen Yang;Po-Lin Kuo;Ming-Shyan Huang.Lung Cancer.2009, 3

[3]

Hypoxic activation of the unfolded protein response (UPR) induces expression of the metastasis-associated gene LAMP3 [J].

Mujcic, Hilda ;

Rzymski, Tomasz ;

Rouschop, Kasper M. A. ;

Koritzinsky, Marianne ;

Milani, Manuela ;

Harris, Adrian L. ;

Wouters, Bradly G. .

RADIOTHERAPY AND ONCOLOGY, 2009, 92 (03) :450-459

[4]

Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells [J].

Bellodi, Cristian ;

Lidonnici, Maria Rosa ;

Hamilton, Ashley ;

Helgason, G. Vignir ;

Soliera, Angela Rachele ;

Ronchetti, Mattia ;

Galavotti, Sara ;

Young, Kenneth W. ;

Selmi, Tommaso ;

Yacobi, Rinat ;

Van Etten, Richard A. ;

Donato, Nick ;

Hunter, Ann ;

Dinsdale, David ;

Tirro, Elena ;

Vigneri, Paolo ;

Nicotera, Pierluigi ;

Dyer, Martin J. ;

Holyoake, Tessa ;

Salomoni, Paolo ;

Calabretta, Bruno .

JOURNAL OF CLINICAL INVESTIGATION, 2009, 119 (05) :1109-1123

[5]

X Box-Binding Protein 1 Regulates Angiogenesis in Human Pancreatic Adenocarcinomas.[J].Lorenzo Romero-Ramirez;Hongbin Cao;Maria Paz Regalado;Neeraja Kambham;Dietmar Siemann;Jeff J. Kim;Quynh T. Le;Albert C. Koong.Translational Oncology.2009, 1

[6]

Benzene activates caspase-4 and-12 at the transcription level, without an association with apoptosis, in mouse bone marrow cells lacking the p53 gene [J].