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• W2415689568 abstract "// Xinyou Xie 1, 2 , Huixing Liu 1, 2 , Yanzhong Wang 1, 2 , Yanwen Zhou 1, 2 , Haitao Yu 1, 2 , Guiling Li 1, 2 , Zhi Ruan 1, 2 , Fengying Li 1, 2 , Xiuhong Wang 1, 2 , Jun Zhang 1, 2 1 Department of Clinical Laboratory, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310016, P.R. China 2 Key Laboratory of Biotherapy of Zhejiang Province, Hangzhou, Zhejiang 310016, P.R. China Correspondence to: Jun Zhang, email: jameszhang2000@163.com Keywords: nicotinamide N-methyltransferase, 1-methylnicotinamide, 5-fluorouracil, colorectal cancer, p38 MAPK Received: October 19, 2015     Accepted: May 30, 2016     Published: June 13, 2016 ABSTRACT Nicotinamide N-methyltransferase (NNMT), which converts nicotinamide to 1-methylnicotinamide (1-MNA), is overexpressed in a variety of human cancers and serves as a potential anti-cancer target. In this study, we investigated the effect of NNMT on 5-fluorouracil (5-FU) sensitivity of colorectal cancer (CRC) cells, and the underlying mechanisms. Our results show that down-regulation of NNMT in CRC HT-29 cells diminishes 5-FU resistance, while over expression of NNMT in SW480 cells enhances it. NNMT reduces reactive oxygen species (ROS) production induced by 5-FU by increasing 1-MNA in CRC cells. The reduction in ROS leads to inactivation of the ASK1-p38 mitogen-activated protein kinase (MAPK) pathway, which reduces 5-FU-induced apoptosis. In vivo , NNMT attenuates 5-FU-induced inhibition of CRC tumor growth in nude mice. These observations suggest that NNMT and the 1-MNA it produces inhibit the ASK1-p38 MAPK pathway, resulting in increased CRC cell resistance to 5-FU." @default.
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• W2415689568 date "2016-06-13" @default.
• W2415689568 modified "2023-09-27" @default.
• W2415689568 title "Nicotinamide N-methyltransferase enhances resistance to 5-fluorouracil in colorectal cancer cells through inhibition of the ASK1-p38 MAPK pathway" @default.
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• W2415689568 doi "https://doi.org/10.18632/oncotarget.9962" @default.
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