The role of tumor suppressor menin in IL-6 regulation in mouse islet tumor cells |
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Authors: | Tae-Yang Song Jihyeon Lim Byungho Kim Jeung-Whan Han Hong-Duk Youn Eun-Jung Cho |
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Affiliation: | 1. School of Pharmacy, Sungkyunkwan University, Suwon, Gyeonggi-do 440-746, Republic of Korea;2. C&C Research Laboratories, Sungkyunkwan University, Suwon, Gyeonggi-do 440-746, Republic of Korea;3. Department of Biomedical Sciences and Biochemistry and Molecular Biology, National Creative Research Center for Epigenome Reprogramming Network, Seoul National University College of Medicine, Seoul 110-799, Republic of Korea |
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Abstract: | Menin is a gene product of multiple endocrine neoplasia type1 (Men1), an inherited familial cancer syndrome characterized by tumors of endocrine tissues. To gain insight about how menin performs an endocrine cell-specific tumor suppressor function, we investigated the possibility that menin was integrated in a cancer-associated inflammatory pathway in a cell type-specific manner. Here, we showed that the expression of IL-6, a proinflammatory cytokine, was specifically elevated in mouse islet tumor cells upon depletion of menin and Men−/− MEF cells, but not in hepatocellular carcinoma cells. Histone H3 lysine (K) 9 methylation, but not H3 K27 or K4 methylation, was involved in menin-dependent IL-6 regulation. Menin occupied the IL-6 promoter and recruited SUV39H1 to induce H3 K9 methylation. Our findings provide a molecular insight that menin-dependent induction of H3 K9 methylation in the cancer-associated interleukin gene might be linked to preventing endocrine-specific tumorigenesis. |
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Keywords: | Menin Tumor suppressor Histone Men1 Histone methylation |
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