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      Therapeutic Effectiveness of Anticancer Phytochemicals on Cancer Stem Cells

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          Abstract

          Understanding how to target cancer stem cells (CSCs) may provide helpful insights for the development of therapeutic or preventive strategies against cancers. Dietary phytochemicals with anticancer properties are promising candidates and have selective impact on CSCs. This review summarizes the influence of phytochemicals on heterogeneous cancer cell populations as well as on specific targeting of CSCs.

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          Evolution of the cancer stem cell model.

          Antonija Kreso, John E. Dick (2014)
          Genetic analyses have shaped much of our understanding of cancer. However, it is becoming increasingly clear that cancer cells display features of normal tissue organization, where cancer stem cells (CSCs) can drive tumor growth. Although often considered as mutually exclusive models to describe tumor heterogeneity, we propose that the genetic and CSC models of cancer can be harmonized by considering the role of genetic diversity and nongenetic influences in contributing to tumor heterogeneity. We offer an approach to integrating CSCs and cancer genetic data that will guide the field in interpreting past observations and designing future studies. Copyright © 2014 Elsevier Inc. All rights reserved.
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            Identification of pancreatic cancer stem cells.

            Chenwei Li, David G Heidt, Piero Dalerba … (2007)
            Emerging evidence has suggested that the capability of a tumor to grow and propagate is dependent on a small subset of cells within a tumor, termed cancer stem cells. Although data have been provided to support this theory in human blood, brain, and breast cancers, the identity of pancreatic cancer stem cells has not been determined. Using a xenograft model in which primary human pancreatic adenocarcinomas were grown in immunocompromised mice, we identified a highly tumorigenic subpopulation of pancreatic cancer cells expressing the cell surface markers CD44, CD24, and epithelial-specific antigen (ESA). Pancreatic cancer cells with the CD44(+)CD24(+)ESA(+) phenotype (0.2-0.8% of pancreatic cancer cells) had a 100-fold increased tumorigenic potential compared with nontumorigenic cancer cells, with 50% of animals injected with as few as 100 CD44(+)CD24(+)ESA(+) cells forming tumors that were histologically indistinguishable from the human tumors from which they originated. The enhanced ability of CD44(+)CD24(+)ESA(+) pancreatic cancer cells to form tumors was confirmed in an orthotopic pancreatic tail injection model. The CD44(+)CD24(+)ESA(+) pancreatic cancer cells showed the stem cell properties of self-renewal, the ability to produce differentiated progeny, and increased expression of the developmental signaling molecule sonic hedgehog. Identification of pancreatic cancer stem cells and further elucidation of the signaling pathways that regulate their growth and survival may provide novel therapeutic approaches to treat pancreatic cancer, which is notoriously resistant to standard chemotherapy and radiation.
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              Highly tumorigenic lung cancer CD133+ cells display stem-like features and are spared by cisplatin treatment.

              Giulia Bertolini, Luca Roz, Paola Perego … (2009)
              The identification of lung tumor-initiating cells and associated markers may be useful for optimization of therapeutic approaches and for predictive and prognostic information in lung cancer patients. CD133, a surface glycoprotein linked to organ-specific stem cells, was described as a marker of cancer-initiating cells in different tumor types. Here, we report that a CD133+, epithelial-specific antigen-positive (CD133+ESA+) population is increased in primary nonsmall cell lung cancer (NSCLC) compared with normal lung tissue and has higher tumorigenic potential in SCID mice and expression of genes involved in stemness, adhesion, motility, and drug efflux than the CD133(-) counterpart. Cisplatin treatment of lung cancer cells in vitro resulted in enrichment of CD133+ fraction both after acute cytotoxic exposure and in cells with stable cisplatin-resistant phenotype. Subpopulations of CD133+ABCG2+ and CD133+CXCR4+ cells were spared by in vivo cisplatin treatment of lung tumor xenografts established from primary tumors. A tendency toward shorter progression-free survival was observed in CD133+ NSCLC patients treated with platinum-containing regimens. Our results indicate that chemoresistant populations with highly tumorigenic and stem-like features are present in lung tumors. The molecular features of these cells may provide the rationale for more specific therapeutic targeting and the definition of predictive factors in clinical management of this lethal disease.
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                Author and article information

                Contributors
                Carmela Fimognari: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Toxins (Basel)
                Journal ID (iso-abbrev): Toxins (Basel)
                Journal ID (publisher-id): toxins
                Title: Toxins
                Publisher: MDPI
                ISSN (Electronic): 2072-6651
                Publication date (Electronic): 30 June 2016
                Publication date Collection: July 2016
                Volume: 8
                Issue: 7
                Electronic Location Identifier: 199
                Affiliations
                [1 ]School of Food Science and Biotechnology (BK21 Plus), Kyungpook National University, Daegu 41566, Korea
                [2 ]Center of Cancer Systems Biology, Tufts University School of Medicine, Boston, MA 02135, USA; hlatky@ 123456cancer-systems-biology.org
                [3 ]Department of Food Science and Technology, Chonbuk National University, Jeonju 54896, Korea; ysjeong@ 123456jbnu.ac.kr
                [4 ]Department of Integrative Physiology and Pathobiology, Tufts University School of Medicine, Boston, MA 02111, USA
                Author notes
                [* ]Correspondence: j.oh@ 123456knu.ac.kr (J.O.); dohoon.kim@ 123456tufts.edu (D.K.); Tel.: +82-53-950-5752 (J.O.); +1-617-519-3530 (D.K.)
                Article
                Publisher ID: toxins-08-00199
                DOI: 10.3390/toxins8070199
                PMC ID: 4963832
                PubMed ID: 27376325
                SO-VID: 4ebabc89-3230-4bdd-ba3d-570793f6bce6
                Copyright © © 2016 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 29 March 2016
                Date accepted : 23 June 2016
                Categories
                Subject: Review

                ScienceOpen disciplines: Molecular medicine
                Keywords: cancer,cancer stem cells,anticancer,phytochemicals,polyphenols
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: cancer, cancer stem cells, anticancer, phytochemicals, polyphenols

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