Mechanism of Cell Adaptation When and How Do Cancer Cells Develop Chemoresistance?

被引:154
作者
Fodale, Valentina [1 ,2 ]
Pierobon, Mariaelena [1 ]
Liotta, Lance [1 ]
Petricoin, Emanuel [1 ]
机构
[1] George Mason Univ, Ctr Appl Prote & Mol Med, Manassas, VA USA
[2] Ist Super Sanita, Physiopathol Genet Dis Sect, Dept Hematol Oncol & Mol Med, I-00161 Rome, Italy
关键词
Proteomics; drug metabolism; intracellular signaling; RESISTANCE-RELATED PROTEIN; II-DIRECTED DRUGS; MULTIDRUG-RESISTANCE; BREAST-CANCER; ACQUIRED-RESISTANCE; KINASE INHIBITORS; COLORECTAL-CANCER; ESTROGEN-RECEPTOR; CARCINOMA-CELLS; GROWTH;
D O I
10.1097/PPO.0b013e318212dd3d
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Chemotherapy treatments are considered essential tools to defeat cancer progression and dissemination to improve patients' quality of life and survival. Although most malignancies initially respond to chemotherapeutic treatments, after an unpredictable period, tumor cells develop mechanisms of resistance to the treatment. Different cell compartments are involved in the mechanism of chemoresistance, and multiple mechanisms can be activated by single cells at different times of the cancer progression. Alteration of drug metabolism, derangement of intracellular pathways' signaling, cross-talk between different membrane receptors, and modification of apoptotic signaling and interference with cell replication are all mechanisms that the cell uses to overcome the effect of pharmacological compounds. In this review, we describe different adaptation, mostly at the level of the proteome, which cancer cells use to develop resistance to cancer treatment.
引用
收藏
页码:89 / 95
页数:7
相关论文
共 66 条
[1]   Multidrug Resistance-Associated Protein 1 (MRP1) mediated vincristine resistance: effects of N-acetylcysteine and Buthionine Sulfoximine [J].
Akan, Ilhan ;
Akan, Selma ;
Akca, Hakan ;
Savas, Burhan ;
Ozben, Tomris .
CANCER CELL INTERNATIONAL, 2005, 5 (1)
[2]   Predictive Molecular Markers of Response to Epidermal Growth Factor Receptor(EGFR) Family-Targeted Therapies [J].
Barton, Sarah ;
Starling, Naureen ;
Swanton, Charles .
CURRENT CANCER DRUG TARGETS, 2010, 10 (08) :799-812
[3]   MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib [J].
Bean, James ;
Brennan, Cameron ;
Shih, Jin-Yuan ;
Riely, Gregory ;
Viale, Agnes ;
Wang, Lu ;
Chitale, Dhananjay ;
Motoi, Noriko ;
Szoke, Janos ;
Broderick, Stephen ;
Balak, Marissa ;
Chang, Wen-Cheng ;
Yu, Chong-Jen ;
Gazdar, Adi ;
Pass, Harvey ;
Rusch, Valerie ;
Gerald, William ;
Huang, Shiu-Feng ;
Yang, Pan-Chyr ;
Miller, Vincent ;
Ladany, Marc ;
Yang, Chih-Hsin ;
Pao, William .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (52) :20932-20937
[4]   Tyrosine kinase receptors as attractive targets of cancer therapy [J].
Bennasroune, A ;
Gardin, A ;
Aunis, D ;
Crémel, G ;
Hubert, P .
CRITICAL REVIEWS IN ONCOLOGY HEMATOLOGY, 2004, 50 (01) :23-38
[5]   Bidirectional cross talk between ERα and EGFR signalling pathways regulates tamoxifen-resistant growth [J].
Britton, D. J. ;
Hutcheson, I. R. ;
Knowlden, J. M. ;
Barrow, D. ;
Giles, M. ;
McClelland, R. A. ;
Gee, J. M. W. ;
Nicholson, R. I. .
BREAST CANCER RESEARCH AND TREATMENT, 2006, 96 (02) :131-146
[6]   Pharmacoproteomic approach to the study of drug mode of action, toxicity, and resistance: applications in diabetes and cancer [J].
Chapal, N ;
Molina, L ;
Molina, F ;
Laplanche, M ;
Pau, B ;
Petit, P .
FUNDAMENTAL & CLINICAL PHARMACOLOGY, 2004, 18 (04) :413-422
[7]   Resistance to chemotherapy and hormone therapy in endometrial cancer [J].
Chaudhry, Parvesh ;
Asselin, Eric .
ENDOCRINE-RELATED CANCER, 2009, 16 (02) :363-380
[8]  
CRUZALEGUI F, 2003, EXPER OPIN THER TAR, V7, P215
[9]   Lung resistance-related protein: Determining its role in multidrug resistance [J].
Dalton, WS ;
Scheper, RJ .
JOURNAL OF THE NATIONAL CANCER INSTITUTE, 1999, 91 (19) :1604-1605
[10]  
de Jong MC, 2001, CANCER RES, V61, P2552