DOI: 10.1002/ame2.12392
Conditional knockout of the NSD2 gene in mouse intestinal epithelial cells inhibits colorectal cancer progression
Mengyuan Li1
Hanxue Chen2
Xingjiu Yang1
Wenlong Zhang1
Chengyan Ma1
Qinghong Wang1
Xinpei Wang1
Ran Gao1
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;NHC Key Laboratory of Human Disease Comparative Medicine,Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases,Beijing,China;Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases,Beijing,China2.Institute of Basic Medical Sciences,Chinese Academy of Medical Sciences,School of Basic Medicine Peking Union Medical College,Beijing,China
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.
机标关键词：knockoutcancercellsmousegenecolorectalconditionalepithelial
论文发表日期：2025-02-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：10( 322-331 )
英文信息