Esophageal cancer prognosis remains poor in current clinical practice. We previously\nreported that moscatilin can induce apoptosis and mitotic catastrophe in esophageal cancer cells,\naccompanied by upregulation of polo-like kinase 1 (Plk1) expression. We aimed to validate in\nvitro activity and Plk1 expression in vivo following moscatilin treatment and to examine the\ntreatmentâ??s radiosensitizing effect. Human esophageal cancer cells were implanted in nude mice.\nMoscatilin was intraperitoneally (i.p.) injected into the mice. Tumor size, body weight, white\nblood cell counts, and liver and renal function were measured. Aberrant mitosis and Plk1\nexpression were assessed. Colony formation was used to measure survival fraction after radiation.\nMoscatilin significantly suppressed tumor growth in mice bearing human esophageal xenografts\nwithout affecting body weight, white blood cell counts, or liver and renal function. Moscatilin also\ninduced aberrant mitosis and apoptosis. Plk1 expression was markedly upregulated in vivo.\nMoreover, moscatilin pretreatment enhanced CE81T/VGH and BE3 cell radioresponse in vitro.\nMoscatilin may inhibit growth of human esophageal tumors and sensitize esophageal cancer cells\nto radiation therapy.
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