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    American journal of cancer research. 2015 Jan 15. pmc: PMC4396035
    Prominin-1 (CD133, AC133) and dipeptidyl-peptidase IV (CD26) are indicators of infinitive growth in colon cancer cells.
    Grunt TW1,  Hebar A2,  Laffer S3,  Wagner R4,  Peter B5,  Herrmann H6,  Graf A7,  Bilban M8,  Posch M9,  Hoermann G10,  Mayerhofer M11,  Eisenwort G12,  Zielinski CC13,  Selzer E14,  Valent P15
    Author information
    1Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria ; Division of Oncology, Department of Medicine I, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    2Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria ; Department of Radiotherapy, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    3Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    4Division of Oncology, Department of Medicine I, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    5Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria ; Department of Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    6Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria ; Department of Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    7Section of Medical Statistics, Center for Medical Statistics, Informatics and Intelligent Systems, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    8Department of Laboratory Medicine, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    9Section of Medical Statistics, Center for Medical Statistics, Informatics and Intelligent Systems, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    10Department of Laboratory Medicine, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    11Department of Laboratory Medicine, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    12Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    13Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria ; Division of Oncology, Department of Medicine I, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    14Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria ; Department of Radiotherapy, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    15Ludwig Boltzmann Cluster Oncology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria ; Department of Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna Waehringer Guertel 18-20, A-1090 Vienna, Austria.
    Abstract

    Advanced colorectal cancer is characterized by uncontrolled growth and resistance against anti-cancer agents, including ErbB inhibitors. Recent data suggest that cancer stem cells (CSC) are particularly resistant. These cells may reside within a CD133+ fraction of the malignant cells. Using HCT116 cells we explored the role of CD133 and other CSC markers in drug resistance in colon cancer cells. CD133+ cells outnumbered CD133- cells over time in long-term culture. Both populations displayed the KRAS mutation 38G > A and an almost identical target profile, including EGFR/ErbB1, ErbB2, and ErbB4. Microarray analyses and flow cytometry identified CD26 as additional CSC marker co-expressed on CD133+ cells. However, knock-down of CD133 or CD26 did not affect short-term growth of HCT116 cells, and both cell-populations were equally resistant to various targeted drugs except irreversible ErbB inhibitors, which blocked growth and ERK1/2 phosphorylation in CD133- cells more efficiently than in CD133+ cells. Moreover, the MEK inhibitor AS703026 was found to overcome resistance against ErbB blockers in CD133+ cells. Together, CD133 and CD26 are markers of long-term growth and resistance to ErbB blockers in HCT116 cells, which may be mediated by constitutive ERK activity.


    KEYWORDS: CD133, CD26, Cancer stem cell, DPPIV, EGFR/ErbB, HCT116, colon cancer, drug resistance

    Publikations ID: 25973297
    Quelle: öffnen
     
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