Conditional knockout of the NSD2 gene in mouse intestinal epithelial cells inhibits colorectal cancer progression
Mengyuan Li, Hanxue Chen, Xingjiu Yang, Wenlong Zhang, Chengyan Ma, Qinghong Wang, Xinpei Wang, Ran Gao- Medical Laboratory Technology
- Veterinary (miscellaneous)
- Molecular Biology
- Biochemistry
- Medicine (miscellaneous)
Abstract
Background
Nuclear receptor‐binding SET domain 2 (NSD2) is a histone methyltransferase, that catalyzes dimethylation of lysine 36 of histone 3 (H3K36me2) and is associated 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 prognosis 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, NSD2fl/fl‐Vil1‐Cre mice exhibited 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.