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作 者:Mengyuan Li Hanxue Chen Xingjiu Yang Wenlong Zhang Chengyan Ma Qinghong Wang Xinpei Wang Ran Gao
机构地区:[1]National Human Diseases Animal Model Resource Center,Institute of Laboratory Animal Science,Chinese Academy of Medical Sciences and Peking Union Medical College,Beijing,China [2]NHC Key Laboratory of Human Disease Comparative Medicine,Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases,Beijing,China [3]Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases,Beijing,China [4]Institute of Basic Medical Sciences,Chinese Academy of Medical Sciences,School of Basic Medicine Peking Union Medical College,Beijing,China
出 处:《Animal Models and Experimental Medicine》2025年第2期322-331,共10页动物模型与实验医学(英文)
基 金:supported by the National Key Research and Development Program of China (2022YFF0710705);the Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences (2021-I2M-1-0 13);funding support from the Special Research Fund for Central Universities;Peking Union Medical College (3332022182);the 111 Project (B20095)
摘 要:Background:Nuclear receptor-binding SET domain 2(NSD2)is a histone methyltrans-ferase,that catalyzes dimethylation of lysine 36 of histone 3(H3K36me2)and is asso-ciated with active transcription of a series of genes.NSD2 is overexpressed in multiple types of solid human tumors and has been proven to be related to unfavorable prog-nosis in several types of tumors.Methods:We established a mouse model in which the NSD2 gene was conditionally knocked out in intestinal epithelial cells.We used azoxymethane and dextran sodium sulfate to chemically induce murine colorectal cancer.The development of colorectal tumors were investigated using post-necropsy quantification,immunohistochemistry,and enzyme-linked immunosorbent assay(ELISA).Results:Compared with wild-type(WT)control mice,NSD2^(fl/fl)-Vil1-Cre mice exhib-ited significantly decreased tumor numbers,histopathological changes,and cytokine expression in colorectal tumors.Conclusions:Conditional knockout of NSD2 in intestinal epithelial cells significantly inhibits colorectal cancer progression.
关 键 词:colorectal cancer NSD2^(fl/fl)-Vil1-Cre mice nuclear receptor-binding SET domain 2
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