Mitosis as an anti-cancer target

被引：90

作者：

Janssen, A. ^{[1
]}

Medema, R. H. ^{[1
]}

机构：

[1] Univ Med Ctr Utrecht, Dept Med Oncol, Canc Genom Ctr, NL-3584 CG Utrecht, Netherlands

来源：

ONCOGENE | 2011年 / 30卷 / 25期

关键词：

mitosis; aneuploidy; CIN; therapy; cancer; SMALL-MOLECULE INHIBITOR; SPINDLE ASSEMBLY CHECKPOINT; CHROMOSOME MIS-SEGREGATION; CELL-CYCLE PROGRESSION; POLO-LIKE KINASE-1; AURORA-B KINASE; GROWTH IN-VIVO; CANCER-CELLS; MITOTIC CHECKPOINT; MAMMALIAN-CELLS;

D O I：

10.1038/onc.2011.30

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Most of the current drugs used to treat cancer can be classified as anti-proliferative drugs. These drugs perturb the proliferative cycle of tumor cells at diverse stages of the cell cycle. Examples of such drugs are DNA-damaging agents and inhibitors of cyclin-dependent kinases that arrest cell cycle progression at different stages of interphase. Another class of anti-proliferative drugs is the so-called anti-mitotic drugs, which selectively perturb progression through mitosis. Mitosis is the shortest and final stage in the cell cycle and has evolved to accurately divide the duplicated genome over the two daughter cells. This review deals with the different strategies that are currently considered to perturb mitotic progression in the treatment of cancer. Oncogene (2011) 30, 2799-2809; doi: 10.1038/onc.2011.30; published online 21 February 2011

引用

页码：2799 / 2809

页数：11

共 131 条

[1] Phosphorylation of caspase-9 by CDK1/cyclin B1 protects mitotic cells against apoptosis [J].

Allan, Lindsey A. ;

Clarke, Paul R. .

MOLECULAR CELL, 2007, 26 (02) :301-310

[2] Polo-like kinase 1 (Plk1) inhibits p53 function by physical interaction and phosphorylation [J].

Ando, K ;

Ozaki, T ;

Yamamoto, H ;

Furuya, K ;

Hosoda, M ;

Hayashi, S ;

Fukuzawa, M ;

Nakagawara, A .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (24) :25549-25561

[3] Tetraploid state induces p53-dependent arrest of nontransformed mammalian cells in G1 [J].

Andreassen, PR ;

Lohez, OD ;

Lacroix, FB ;

Margolis, RL .

MOLECULAR BIOLOGY OF THE CELL, 2001, 12 (05) :1315-1328

[4] Whole Chromosome Instability Caused by Bub1 Insufficiency Drives Tumorigenesis through Tumor Suppressor Gene Loss of Heterozygosity [J].

Baker, Darren J. ;

Jin, Fang ;

Jeganathan, Karthik B. ;

van Deursen, Jan M. .

CANCER CELL, 2009, 16 (06) :475-486

[5] Chromatid cohesion defects may underlie chromosome instability in human colorectal cancers [J].

Barber, Thomas D. ;

McManus, Kirk ;

Yuen, Karen W. Y. ;

Reis, Marcelo ;

Parmigiani, Giovanni ;

Shen, Dong ;

Barrett, Irene ;

Nouhi, Yasaman ;

Spencer, Forrest ;

Markowitz, Sanford ;

Velculescu, Victor E. ;

Kinzler, Kenneth W. ;

Vogelstein, Bert ;

Lengauer, Christoph ;

Hieter, Philip .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (09) :3443-3448

[6] Polo-like kinases and the orchestration of cell division [J].

Barr, FA ;

Silljé, HHW ;

Nigg, EA .

NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2004, 5 (06) :429-440

[7] Cytokinesis: Placing and making the final cut [J].

Barr, Francis A. ;

Gruneberg, Ulrike .

CELL, 2007, 131 (05) :847-860

[8] Centrosome amplification can initiate tumorigenesis in flies [J].

Basto, Renata ;

Brunk, Kathrin ;

Vinadogrova, Tatiana ;

Peel, Nina ;

Franz, Anna ;

Khodjakov, Alexey ;

Raff, Jordan W. .

CELL, 2008, 133 (06) :1032-1042

[9] Phosphorylation by p34(cdc2) regulates spindle association of human Eg5, a kinesin-related motor essential for bipolar spindle formation in vivo [J].

Blangy, A ;

Lane, HA ;

dHerin, P ;

Harper, M ;

Kress, M ;

Nigg, EA .

CELL, 1995, 83 (07) :1159-1169

[10]

Boveri T, 1914, FRAGE ENTSTEHUNG MAL, V1

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