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Literature summary for 2.1.1.1 extracted from

  • Xie, X.; Liu, H.; Wang, Y.; Zhou, Y.; Yu, H.; Li, G.; Ruan, Z.; Li, F.; Wang, X.; Zhang, J.
    Nicotinamide N-methyltransferase enhances resistance to 5-fluorouracil in colorectal cancer cells through inhibition of the ASK1-p38 MAPK pathway (2016), Oncotarget, 7, 45837-45848 .
    View publication on PubMedView publication on EuropePMC
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Application

Application Comment Organism
medicine down-regulation of NNMT in colorectal cancer HT-29 cells diminishes 5-fluorouracil resistance, while overexpression of NNMT in SW-480 cells enhances it Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens P40261
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Source Tissue

Source Tissue Comment Organism Textmining
HT-29 cell
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 Homo sapiens
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SW-480 cell
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 Homo sapiens
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General Information

General Information Comment Organism
physiological function down-regulation of NNMT in colorectal cancer HT-29 cells diminishes 5-fluorouracil resistance, while overexpression of NNMT in SW-480 cells enhances it. NNMT reduces reactive oxygen species production induced by 5-fluorouracil by increasing 1-methylnicotinamide in colorectal cancer cells. The reduction in ROS leads to inactivation of the ASK1-p38 mitogen-activated protein kinase pathway, which reduces 5-fluorouracil-induced apoptosis. In nude mice implanted with colorectal cancer xenografts, NNMT attenuates 5-fluorouracil-induced inhibition of colorectal cancer tumor growth Homo sapiens