Cancer Stem Cell Quiescence and Plasticity as Major Challenges in Cancer Therapy

被引:288
作者
Chen, Wanyin [1 ]
Dong, Jihu [1 ]
Haiech, Jacques [1 ]
Kilhoffer, Marie-Claude [1 ]
Zeniou, Maria [1 ]
机构
[1] Univ Strasbourg, Lab Innovat Therapeut, CNRS UMR7200, Lab Excellence Medalis,Fac Pharm, 74 Route Rhin, F-67401 Illkirch Graffenstaden, France
关键词
EPITHELIAL-MESENCHYMAL TRANSITION; PANCREATIC STELLATE CELLS; HYPOXIA-INDUCIBLE FACTORS; TUMOR-INITIATING CELLS; ACUTE MYELOID-LEUKEMIA; OVARIAN-CANCER; PROSPECTIVE IDENTIFICATION; EPIGENETIC REGULATION; EXTRACELLULAR-MATRIX; SIGNALING PATHWAYS;
D O I
10.1155/2016/1740936
中图分类号
Q813 [细胞工程];
学科分类号
摘要
Cells with stem-like properties, tumorigenic potential, and treatment-resistant phenotypes have been identified in many human malignancies. Based on the properties they share with nonneoplastic stem cells or their ability to initiate and propagate tumors in vivo, such cells were designated as cancer stem (stem-like) or tumor initiating/propagating cells. Owing to their implication in treatment resistance, cancer stem cells (CSCs) have been the subject of intense investigation in past years. Comprehension of CSCs' intrinsic properties and mechanisms they develop to survive and even enhance their aggressive phenotype within the hostile conditions of the tumor microenvironment has reoriented therapeutic strategies to fight cancer. This report provides selected examples of malignancies in which the presence of CSCs has been evidenced and briefly discusses methods to identify, isolate, and functionally characterize the CSC subpopulation of cancer cells. Relevant biological targets in CSCs, their link to treatment resistance, proposed targeting strategies, and limitations of these approaches are presented. Two major aspects of CSC physiopathology, namely, relative in vivo quiescence and plasticity in response to microenvironmental cues or treatment, are highlighted. Implications of these findings in the context of the development of new therapies are discussed.
引用
收藏
页数:16
相关论文
共 166 条
[1]   Computational Identification of a p38SAPK-Regulated Transcription Factor Network Required for Tumor Cell Quiescence [J].
Adam, Alejandro P. ;
George, Ajish ;
Schewe, Denis ;
Bragado, Paloma ;
Iglesias, Bibiana V. ;
Ranganathan, Aparna C. ;
Kourtidis, Antonis ;
Conklin, Douglas S. ;
Aguirre-Ghiso, Julio A. .
CANCER RESEARCH, 2009, 69 (14) :5664-5672
[2]   Prospective identification of tumorigenic breast cancer cells [J].
Al-Hajj, M ;
Wicha, MS ;
Benito-Hernandez, A ;
Morrison, SJ ;
Clarke, MF .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (07) :3983-3988
[3]   Conversion to stem-cell state in response to microenvironmental cues is regulated by balance between epithelial and mesenchymal features in lung cancer cells [J].
Andriani, Francesca ;
Bertolini, Giulia ;
Facchinetti, Federica ;
Baldoli, Erika ;
Moro, Massimo ;
Casalini, Patrizia ;
Caserini, Roberto ;
Milione, Massimo ;
Leone, Giorgia ;
Pelosi, Giuseppe ;
Pastorino, Ugo ;
Sozzi, Gabriella ;
Roz, Luca .
MOLECULAR ONCOLOGY, 2016, 10 (02) :253-271
[4]   The epigenetics of tumour initiation: cancer stem cells and their chromatin [J].
Avgustinova, Alexandra ;
Aznar Benitah, Salvador .
CURRENT OPINION IN GENETICS & DEVELOPMENT, 2016, 36 :8-15
[5]   Epigenetic regulation of CD133 and tumorigenicity of CD133+ovarian cancer cells [J].
Baba, T. ;
Convery, P. A. ;
Matsumura, N. ;
Whitaker, R. S. ;
Kondoh, E. ;
Perry, T. ;
Huang, Z. ;
Bentley, R. C. ;
Mori, S. ;
Fujii, S. ;
Marks, J. R. ;
Berchuck, A. ;
Murphy, S. K. .
ONCOGENE, 2009, 28 (02) :209-218
[6]   Identification of a population of blood circulating tumor cells from breast cancer patients that initiates metastasis in a xenograft assay [J].
Baccelli, Irene ;
Schneeweiss, Andreas ;
Riethdorf, Sabine ;
Stenzinger, Albrecht ;
Schillert, Anja ;
Vogel, Vanessa ;
Klein, Corinna ;
Saini, Massimo ;
Baeuerle, Tobias ;
Wallwiener, Markus ;
Holland-Letz, Tim ;
Hoefner, Thomas ;
Sprick, Martin ;
Scharpff, Martina ;
Marme, Frederik ;
Sinn, Hans Peter ;
Pantel, Klaus ;
Weichert, Wilko ;
Trumpp, Andreas .
NATURE BIOTECHNOLOGY, 2013, 31 (06) :539-U143
[7]   Aberrant mesenchymal differentiation of glioma stem-like cells: implications for therapeutic targeting [J].
Balasubramaniyan, Veerakumar ;
Vaillant, Brian ;
Wang, Shuzhen ;
Gumin, Joy ;
Butalid, M. Elena ;
Sai, Ke ;
Mukheef, Farah ;
Kim, Se Hoon ;
Boddeke, H. W. G. M. ;
Lang, Frederick ;
Aldape, Kenneth ;
Sulman, Erik P. ;
Bhat, Krishna P. ;
Colman, Howard .
ONCOTARGET, 2015, 6 (31) :31007-31017
[8]   Cancer stem cells: a metastasizing menace! [J].
Bandhavkar, Saurabh .
CANCER MEDICINE, 2016, 5 (04) :649-655
[9]   Glioma stem cells promote radioresistance by preferential activation of the DNA damage response [J].
Bao, Shideng ;
Wu, Qiulian ;
McLendon, Roger E. ;
Hao, Yueling ;
Shi, Qing ;
Hjelmeland, Anita B. ;
Dewhirst, Mark W. ;
Bigner, Darell D. ;
Rich, Jeremy N. .
NATURE, 2006, 444 (7120) :756-760
[10]   HYPOXIA AND METABOLISM SERIES - TIMELINE The impact of O2 availability on human cancer [J].
Bertout, Jessica A. ;
Patel, Shetal A. ;
Simon, M. Celeste .
NATURE REVIEWS CANCER, 2008, 8 (12) :967-975