@entity3323 is formed during cooking processes and is present in many foods. Accumulating evidence suggests that @entity5066 is carcinogenic, but the underlying mechanism remains unclear. Here, we investigated the carcinogenesis mechanisms of @entity5066 . @entity5066 increased the @entity10178 expression. Two major transcription factors, AP-1 and NF-kB, were activated by @entity5066 treatment. @entity5066 induced the ERK phosphorylation, and this was abolished by the treatment of @entity5732 , a pharmacological inhibitor of @entity13438 , an upstream kinase of ERK. @entity5066 -induced expression and promoter activity of @entity10178 were suppressed by @entity5732 . @entity5732 treatment attenuated @entity5066 -induced transactivation of AP-1 and NF-kB, suggesting that the @entity13438 /ERK signaling pathway regulates @entity10178 expression. In addition, @entity3091 , a natural inhibitor of the @entity13438 /ERK signal pathway, reduced @entity5066 -induced activation of the @entity10178 promoter as well as activation of AP-1 and NF-kB. Collectively, these results suggest that the ability of @entity5066 to up-regulate @entity10178 expression through the @entity13438 /ERK signaling pathway underlies @entity5066 .

XXXX up-regulates cyclooxygenase-2 expression through the @entity13438 /ERK signaling pathway in mouse epidermal cells.

@entity3091 :: ('MESH:C040015', 'Chemical') :: ['myricetin'] @entity10178 :: ('17709(Tax:10090)', 'Gene') :: ['COX-2'] @entity5066 :: ('MESH:C566236', 'Disease') :: ['AA', 'AA carcinogenicity'] @entity5732 :: ('MESH:C113580', 'Chemical') :: ['U0126'] @entity13438 :: ('17242(Tax:10090)', 'Gene') :: ['MEK'] @entity3323 :: ('MESH:D020106', 'Chemical') :: ['Acrylamide']
@entity3323 :: (MESH:D020106,Chemical) :: ['Acrylamide']
