Activation and role of caspases in chemotherapy-induced apoptosis

被引：25

作者：

Schmitt, E ^{[1
]}

Sané, AT ^{[1
]}

Bertand, R ^{[1
]}

机构：

[1] Univ Montreal, Hosp Res Ctr, Notre Dame Hosp, Inst Canc Montreal, Montreal, PQ H2L 4M1, Canada

来源：

DRUG RESISTANCE UPDATES | 1999年 / 2卷 / 01期

基金：

英国医学研究理事会;

关键词：

D O I：

10.1054/drup.1999.0065

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

The importance of caspase activation during apoptosis has become eminently apparent in the last few years. The caspases participate in a proteolytic cascade activated in response to various stimuli, including anticancer drugs, that results in the systematic and orderly eradication of the cell. The core machinery of caspase activation is now emerging and involves multiple molecular complexes. We describe the two best-studied models of caspase activation, the mitochondrial pathway and the cell death receptor pathway, and discuss their involvement in caspase activation induced by various anticancer drugs used in chemotherapy. Defective apoptosis contributes to tumor growth and drug resistance. Understanding the activation and role of caspases in apoptosis may help develop new therapeutic strategies to circumvent drug resistance.

引用

页码：21 / 29

页数：9

共 85 条

[1]

Alnemri ES, 1997, J CELL BIOCHEM, V64, P33, DOI 10.1002/(SICI)1097-4644(199701)64:1<33::AID-JCB6>3.0.CO

[2]

2-0

[3] Death receptors: Signaling and modulation [J].

Ashkenazi, A ;

Dixit, VM .

SCIENCE, 1998, 281 (5381) :1305-1308

[4] ONCOGENES AND THE STRATEGY OF GROWTH-FACTORS [J].

BASERGA, R .

CELL, 1994, 79 (06) :927-930

[5] Defects in regulation of apoptosis in caspase-2-deficient mice [J].

Bergeron, L ;

Perez, GI ;

Macdonald, G ;

Shi, LF ;

Sun, Y ;

Jurisicova, A ;

Varmuza, S ;

Latham, KE ;

Flaws, JA ;

Salter, JCM ;

Hara, H ;

Moskowitz, MA ;

Li, E ;

Greenberg, A ;

Tilly, JL ;

Yuan, JY .

GENES & DEVELOPMENT, 1998, 12 (09) :1304-1314

[6] Bcl-x(L) can inhibit apoptosis in cells that have undergone Fas-induced protease activation [J].

Boise, LH ;

Thompson, CB .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (08) :3759-3764

[7] Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization [J].

Bossy-Wetzel, E ;

Newmeyer, DD ;

Green, DR .

EMBO JOURNAL, 1998, 17 (01) :37-49

[8] Apaf1 (CED-4 homolog) regulates programmed cell death in mammalian development [J].

Cecconi, F ;

Alvarez-Bolado, G ;

Meyer, BI ;

Roth, KA ;

Gruss, P .

CELL, 1998, 94 (06) :727-737

[9] BCL-2 FAMILY: Regulators of cell death [J].

Chao, DT ;

Korsmeyer, SJ .

ANNUAL REVIEW OF IMMUNOLOGY, 1998, 16 :395-419

[10] Interaction of CED-4 with CED-3 and CED-9: A molecular framework for cell death [J].

Chinnaiyan, AM ;

ORourke, K ;

Lane, BR ;

Dixit, VM .

SCIENCE, 1997, 275 (5303) :1122-1126

← 1 2 3 4 5 6 7 8 9 →