Defective acute apoptotic response to genotoxic carcinogen in small intestine of APCMin/+ mice is restored by sulindac

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    Abstract

    The effect of APC loss on azoxymethane (AOM)-induced apoptosis and cell proliferation, as well as their regulation by sulindac was examined in colon and small intestine in APCMin/+ mice. APCMin/+ mice showed increased epithelial proliferation in all regions, with significant impairment of apoptosis in small intestine, but not in colon. Sulindac administration restored defective apoptosis to normal. As the apoptotic defect occurred at the major site of intestinal tumor formation in APCMin/+ mice and as it was restored to normal by a proven chemopreventive agent, this defect in apoptosis might be a key biological consequence of APC dysfunction contributing to tumor formation.

    Original languageEnglish
    Pages (from-to)234-244
    Number of pages11
    JournalCancer Letters
    Volume248
    Issue number2
    DOIs
    Publication statusPublished - 18 Apr 2007

    Keywords

    • APC
    • Apoptosis
    • Cell proliferation
    • Colorectal cancer
    • Genotoxic carcinogen
    • Sulindac

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