Calcium Prevents Tumorigenesis in a Mouse Model of Colorectal Cancer 英文参考文献.docVIP

CalciumPreventsTumorigenesisinaMouseModelof ColorectalCancer Ji-LinWang1.,Yan-WeiLin1.,Hui-MinChen1,XuanKong1,HuaXiong1,NanShen2,JieHong1 ,Jing-Yuan Fang1* 1 Division of Gastroenterology, Shanghai Jiao-Tong University School of Medicine, Renji Hospital, Shanghai Institute of Digestive Disease, Shanghai, China,2 Division of Rheumatology, Shanghai Jiao-Tong University School of Medicine, Renji Hospital, Shanghai, China Abstract BackgroundandAim: Calcium has been proposed as a mediator of the chemoprevention of colorectal cancer (CRC), but the comprehensive mechanism underlying this preventive effect is not yet clear. Hence, we conducted this study to evaluate the possible roles and mechanisms of calcium-mediated prevention of CRC induced by 1,2-dimethylhydrazine (DMH) in mice. Methods: For gene expression analysis, 6 non-tumor colorectal tissues of mice from the DMH + Calcium group and 3 samples each from the DMH and control groups were hybridized on a 4644 K Agilent whole genome oligo microarray, and selected genes were validated by real-time polymerase chain reaction (PCR). Functional analysis of the microarray data was performed using KEGG and Gene Ontology (GO) analyses. Hub genes were identified using Pathway Studio software. Results: The tumor incidence rates in the DMH and DMH+ Calcium groups were 90% and 40%, respectively. Microarray gene expression analysis showed that S100a9, Defa20, Mmp10, Mmp7, Ptgs2, and Ang2 were among the most downregulated genes, whereas Per3, Tef, Rnf152, and Prdx6 were significantly upregulated in the DMH + Calcium group compared with the DMH group. Functional analysis showed that the Wnt, cell cycle, and arachidonic acid pathways were significantly downregulated in the DMH+ Calcium group, and that the GO terms related to cell differentiation, cell cycle, proliferation, cell dea