Oncogenic role of kinesin proteins and targeting kinesin therapy

被引:131
作者
Liu, Xinran [1 ]
Gong, Hao [1 ]
Huang, Kun [1 ,2 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Sch Pharm, Wuhan 430074, Peoples R China
[2] Wuhan Inst Biotechnol, Ctr Biomed Res, Wuhan, Peoples R China
关键词
CENTROMERE-ASSOCIATED KINESIN; MESSENGER-RNA EXPRESSION; SMALL-MOLECULE INHIBITOR; PHASE-I TRIAL; CENP-E; HEDGEHOG PATHWAY; DOSE-ESCALATION; GENE-EXPRESSION; TUMOR-FORMATION; CANCER CELLS;
D O I
10.1111/cas.12138
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The kinesin superfamily (KIF) is a group of proteins that share a highly conserved motor domain. Except for some members, many KIF proteins have adenosine triphosphatase activity and microtubule-dependent plus-end motion ability. Kinesins participate in several essential cellular functions, including mitosis, meiosis and the transport of macromolecules. Increasing evidence indicates kinesin proteins play critical roles in the genesis and development of human cancers. Some kinesin proteins are associated with maligancy as well as drug resistance of solid tumor. Thus, targeting KIF therapy seems to be a promising anticancer strategy. Inhibitors of KIF such as kinesin spindle protein (KSP/Eg5) have entered clinical trials for monotherapy or in combination with other drugs, and kinesins other than Eg5 with various potential anticancer target characteristics are also constantly being discovered and studied. Here, we summarize the oncogenic roles of kinesin proteins and potential cancer therapy strategies that target KIF.
引用
收藏
页码:651 / 656
页数:6
相关论文
共 81 条
[1]   Consensus transcriptome signature of perineural invasion in pancreatic carcinoma [J].
Abiatari, Ivane ;
DeOliveira, Tiago ;
Kerkadze, Vachtang ;
Schwager, Christian ;
Esposito, Irene ;
Giese, Nathalia A. ;
Huber, Peter ;
Bergman, Frank ;
Abdollahi, Amir ;
Friess, Helmut ;
Kleeff, Joerg .
MOLECULAR CANCER THERAPEUTICS, 2009, 8 (06) :1494-1504
[2]  
[Anonymous], 2003, COMMON TERMINOLOGY C
[3]   Kinesin family member 2C (KIF2C/MCAK) is a novel marker for prognosis in human gliomas [J].
Bie, Li ;
Zhao, Gang ;
Wang, Yin-ping ;
Zhang, Bo .
CLINICAL NEUROLOGY AND NEUROSURGERY, 2012, 114 (04) :356-360
[4]   A phase I trial of ispinesib, a kinesin spindle protein inhibitor, with docetaxel in patients with advanced solid tumours [J].
Blagden, S. P. ;
Molife, L. R. ;
Seebaran, A. ;
Payne, M. ;
Reid, A. H. M. ;
Protheroe, A. S. ;
Vasist, L. S. ;
Williams, D. D. ;
Bowen, C. ;
Kathman, S. J. ;
Hodge, J. P. ;
Dar, M. M. ;
de Bono, J. S. ;
Middleton, M. R. .
BRITISH JOURNAL OF CANCER, 2008, 98 (05) :894-899
[5]   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
[6]   Overexpression of Eg5 causes genomic instability and tumor formation in mice [J].
Castillo, Andrew ;
Morse, Herbert C., III ;
Godfrey, Virginia L. ;
Naeem, Rizwan ;
Justice, Monica J. .
CANCER RESEARCH, 2007, 67 (21) :10138-10147
[7]   First-time-in-human study of GSK923295, a novel antimitotic inhibitor of centromere-associated protein E (CENP-E), in patients with refractory cancer [J].
Chung, Vincent ;
Heath, Elisabeth I. ;
Schelman, William R. ;
Johnson, Brendan M. ;
Kirby, Lyndon C. ;
Lynch, Kerlin M. ;
Botbyl, JeVrey D. ;
Lampkin, Thomas A. ;
Holen, Kyle D. .
CANCER CHEMOTHERAPY AND PHARMACOLOGY, 2012, 69 (03) :733-741
[8]   KIF14 messenger RNA expression is independently prognostic for outcome in lung cancer [J].
Corson, Timothy W. ;
Zhu, Chang Qi ;
Lau, Suzanne K. ;
Shepherd, Frances A. ;
Tsao, Ming-Sound ;
Gallie, Brenda L. .
CLINICAL CANCER RESEARCH, 2007, 13 (11) :3229-3234
[9]   KIF14 mRNA expression is a predictor of grade and outcome in breast cancer [J].
Corson, Timothy W. ;
Gallie, Brenda L. .
INTERNATIONAL JOURNAL OF CANCER, 2006, 119 (05) :1088-1094
[10]   KIF14 is a candidate oncogene in the 1q minimal region of genomic gain in multiple cancers [J].
Corson, TW ;
Huang, A ;
Tsao, MS ;
Gallie, BL .
ONCOGENE, 2005, 24 (30) :4741-4753