偶氮甲烷
癌变
生物
结直肠癌
癌症研究
细胞生长
激酶
结肠炎
基因剔除小鼠
大肠癌小鼠模型的建立
磷酸酶
碳酸钙-2
细胞培养
癌症
免疫学
基因
细胞生物学
磷酸化
遗传学
作者
Chin Wen Png,Madhushanee Weerasooriya,Jun Guo,Sharmy J. James,Han-Ming Poh,Motomi Osato,Richard A. Flavell,Chen Dong,Henry Yang,Ye Zhang
出处
期刊:Oncogene
[Springer Nature]
日期:2015-03-16
卷期号:35 (2): 206-217
被引量:38
摘要
Dual specificity phosphatase 10 (DUSP10), also known as MAP kinase phosphatase 5 (MKP5), negatively regulates the activation of MAP kinases. Genetic polymorphisms and aberrant expression of this gene are associated with colorectal cancer (CRC) in humans. However, the role of DUSP10 in intestinal epithelial tumorigenesis is not clear. Here, we showed that DUSP10 knockout (KO) mice had increased intestinal epithelial cell (IEC) proliferation and migration and developed less severe colitis than wild-type (WT) mice in response to dextran sodium sulphate (DSS) treatment, which is associated with increased ERK1/2 activation and Krüppel-like factor 5 (KLF5) expression in IEC. In line with increased IEC proliferation, DUSP10 KO mice developed more colon tumours with increased severity compared with WT mice in response to administration of DSS and azoxymethane (AOM). Furthermore, survival analysis of CRC patients demonstrated that high DUSP10 expression in tumours was associated with significant improvement in survival probability. Overexpression of DUSP10 in Caco-2 and RCM-1 cells inhibited cell proliferation. Our study showed that DUSP10 negatively regulates IEC growth and acts as a suppressor for CRC. Therefore, it could be targeted for the development of therapies for colitis and CRC.
科研通智能强力驱动
Strongly Powered by AbleSci AI