Targeting Ras and Rho GTPases as opportunities for cancer therapeutics

被引:110
作者
Walker, K [1 ]
Olson, MF [1 ]
机构
[1] Beatson Inst Canc Res, Glasgow G61 1BD, Lanark, Scotland
关键词
D O I
10.1016/j.gde.2004.11.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The Ras and Rho GTPases contribute to the initiation and progression of cancer by subverting the normal regulation of specific intracellular signalling pathways. As a result, Ras and Rho play significant roles in the development of numerous aspects of the malignant phenotype by promoting cell cycle progression, resistance to apoptotic stimuli, neovascularisation and tumour cell motility, invasiveness and metastasis. With these GTPases contributing at so many levels, they are appealing targets for the development of cancer chemotherapeutic agents.
引用
收藏
页码:62 / 68
页数:7
相关论文
共 52 条
[1]   Guanosine triphosphatase stimulation of oncogenic Ras mutants [J].
Ahmadian, MR ;
Zor, T ;
Vogt, D ;
Kabsch, W ;
Selinger, Z ;
Wittinghofer, A ;
Scheffzek, K .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (12) :7065-7070
[2]   Inactivation of Icmt inhibits transformation by oncogenic K-Ras and B-Raf [J].
Bergo, MO ;
Gavino, BJ ;
Hong, C ;
Beigneux, AP ;
McMahon, M ;
Casey, PJ ;
Young, SG .
JOURNAL OF CLINICAL INVESTIGATION, 2004, 113 (04) :539-550
[3]   Absence of the CAAX endoprotease Rce1: Effects on cell growth and transformation [J].
Bergo, MO ;
Ambroziak, P ;
Gregory, C ;
George, A ;
Otto, JC ;
Kim, E ;
Nagase, H ;
Casey, PJ ;
Balmain, A ;
Young, SG .
MOLECULAR AND CELLULAR BIOLOGY, 2002, 22 (01) :171-181
[4]   Targeted inactivation of the isoprenylcysteine carboxyl methyltransferase gene causes mislocalization of K-Ras in mammalian cells [J].
Bergo, MO ;
Leung, GK ;
Ambroziak, P ;
Otto, JC ;
Casey, PJ ;
Young, SG .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (23) :17605-17610
[5]  
Britten CD, 2001, CLIN CANCER RES, V7, P3894
[6]   High-performance liquid chromatography/mass spectrometry characterization of Ki4B-Ras in PSN-1 cells treated with the prenyltransferase inhibitor L-778,123 [J].
Buser, CA ;
Dinsmore, CJ ;
Fernandes, C ;
Greenberg, I ;
Hamilton, K ;
Mosser, SD ;
Walsh, ES ;
Williams, TM ;
Koblan, KS .
ANALYTICAL BIOCHEMISTRY, 2001, 290 (01) :126-137
[7]   The farnesyl transferase inhibitor R115777 (Zarnestra®) synergistically enhances growth inhibition and apoptosis induced on epidermoid cancer cells by Zoledronic acid (Zometa®) and Pamidronate [J].
Caraglia, M ;
D'Alessandro, AM ;
Marra, M ;
Giuberti, G ;
Vitale, G ;
Viscomi, C ;
Colao, A ;
Del Prete, S ;
Tagliaferri, P ;
Tassone, P ;
Budillon, A ;
Venuta, S ;
Abbruzzese, A .
ONCOGENE, 2004, 23 (41) :6900-6913
[8]   RAS and RHO GTPases in G1-phase cell-cycle regulation [J].
Coleman, ML ;
Marshall, CJ ;
Olson, MF .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2004, 5 (05) :355-366
[9]   Neurofibromatosis 1: closing the GAP between mice and men [J].
Dasgupta, B ;
Gutmann, DH .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 2003, 13 (01) :20-27
[10]   New insights into the actions of bisphosphonate zoledronic acid in breast cancer cells by dual RhoA-dependent and -independent effects [J].
Denoyelle, C ;
Hong, L ;
Vannier, JP ;
Soria, J ;
Soria, C .
BRITISH JOURNAL OF CANCER, 2003, 88 (10) :1631-1640