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      Glycosylation of Cancer Stem Cells: Function in Stemness, Tumorigenesis, and Metastasis

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          Abstract

          Aberrant glycosylation plays a critical role in tumor aggressiveness, progression, and metastasis. Emerging evidence associates cancer initiation and metastasis to the enrichment of cancer stem cells (CSCs). Several universal markers have been identified for CSCs characterization; however, a specific marker has not yet been identified for different cancer types. Specific glycosylation variation plays a major role in the progression and metastasis of different cancers. Interestingly, many of the CSC markers are glycoproteins and undergo differential glycosylation. Given the importance of CSCs and altered glycosylation in tumorigenesis, the present review will discuss current knowledge of altered glycosylation of CSCs and its application in cancer research.

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          Epithelial-mesenchymal transitions in development and disease.

          Jean Paul Thiery, Hervé Acloque, Ruby Y J Huang … (2009)
          The epithelial to mesenchymal transition (EMT) plays crucial roles in the formation of the body plan and in the differentiation of multiple tissues and organs. EMT also contributes to tissue repair, but it can adversely cause organ fibrosis and promote carcinoma progression through a variety of mechanisms. EMT endows cells with migratory and invasive properties, induces stem cell properties, prevents apoptosis and senescence, and contributes to immunosuppression. Thus, the mesenchymal state is associated with the capacity of cells to migrate to distant organs and maintain stemness, allowing their subsequent differentiation into multiple cell types during development and the initiation of metastasis.
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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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              Assembly of asparagine-linked oligosaccharides.

              R Kornfeld, S. Kornfeld (1985)
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                Author and article information

                Contributors
                Srikanth Barkeer
                Seema Chugh
                Surinder K Batra
                Moorthy P. Ponnusamy
                Journal
                Journal ID (nlm-ta): Neoplasia
                Journal ID (iso-abbrev): Neoplasia
                Title: Neoplasia (New York, N.Y.)
                Publisher: Neoplasia Press
                ISSN (Print): 1522-8002
                ISSN (Electronic): 1476-5586
                Publication date PMC-release: 06 July 2018
                Publication date Collection: August 2018
                Publication date (Electronic): 06 July 2018
                Volume: 20
                Issue: 8
                Pages: 813-825
                Affiliations
                [* ]Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE
                [† ]Fred and Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198, USA
                Author notes
                [* ]Address all correspondence to: Moorthy P. Ponnusamy, PhD, or Surinder K. Batra, PhD, Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska, 68198-5870, U.S.A. sbatra@ 123456unmc.edu mpalanim@ 123456unmc.edu
                Article
                Publisher ID: S1476-5586(18)30181-7
                DOI: 10.1016/j.neo.2018.06.001
                PMC ID: 6037882
                PubMed ID: 30015157
                SO-VID: 160ef67c-abc7-4880-9d32-82dbefd9a24a
                Copyright © © 2018 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 28 March 2018
                Date revision received : 1 June 2018
                Date accepted : 11 June 2018
                Categories
                Subject: Review article

                Data availability:

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