原创力文档reduced intestinal tumorigenesis in apcmin mice lacking melanin-concentrating hormone减少肠道肿瘤发生在apcmin老鼠缺乏melanin-concentrating激素.pdfVIP
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reduced intestinal tumorigenesis in apcmin mice lacking melanin-concentrating hormone减少肠道肿瘤发生在apcmin老鼠缺乏melanin-concentrating激素
Reduced Intestinal Tumorigenesis in APCmin Mice
Lacking Melanin-Concentrating Hormone
Jutta M. Nagel, Brenda M. Geiger, Apostolos K. A. Karagiannis, Beatriz Gras-Miralles, David Horst,
Robert M. Najarian, Dimitrios C. Ziogas, XinHua Chen, Efi Kokkotou*
Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America
Abstract
Background: Melanin-concentrating hormone (MCH) is an evolutionary conserved hypothalamic neuropeptide that in
mammals primarily regulates appetite and energy balance. We have recently identified a novel role for MCH in intestinal
inflammation by demonstrating attenuated experimental colitis in MCH deficient mice or wild type mice treated with an
anti-MCH antibody. Therefore, targeting MCH has been proposed for the treatment of inflammatory bowel disease. Given
the link between chronic intestinal inflammation and colorectal cancer, in the present study we sought to investigate
whether blocking MCH might have effects on intestinal tumorigenesis that are independent of inflammation.
Methodology: Tumor development was evaluated in MCH-deficient mice crossed to the APCmin mice which develop
spontaneously intestinal adenomas. A different cohort of MCH 2/ 2 and MCH+/+ mice in the APCmin background was
treated with dextran sodium sulphate (DSS) to induce inflammation-dependent colorectal tumors. In Caco2 human
colorectal adenocarcinoma cells, the role of MCH on cell survival, proliferation and apoptosis was investigated.
Results: APCmin mice lacking MCH developed fewer, smaller and less dysplastic tumors in the intestine and colon which at
the molecular level are characterized by attenuated activation of the wnt/beta-catenin signaling pathway and increased
apoptotic indices. Form a mechanistic po
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