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- W2024531728 abstract "In the present study, we examined a role of mitogen-activated protein kinases (MAPKs), extracellular signal-related kinase (ERK), c-Jun N-terminal protein kinase, and p38 MAPK in troglitazone-induced inhibition of cell growth in human pancreatic cancer cells. Among the three kinases, troglitazone specifically inhibited the phosphorylation of ERK1/2 in a dose- and time-dependent manner. Troglitazone also down-regulated the protein expression of mitogen-activated protein kinase kinase (MEK)1/2, an upstream molecule that regulates ERK phosphorylation. Treatment of human pancreatic cancer cells with specific MEK inhibitor, PD98059 or U0126, inhibited ERK1/2 phosphorylation and cell growth. These results suggest for the first time that the inhibition of the MEK1/2–ERK1/2 signaling pathway may be implicated in the growth inhibitory effect by troglitazone in human pancreatic cancer cells." @default.
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- W2024531728 date "2005-06-01" @default.
- W2024531728 modified "2023-10-16" @default.
- W2024531728 title "Involvement of MEK–ERK signaling pathway in the inhibition of cell growth by troglitazone in human pancreatic cancer cells" @default.
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- W2024531728 doi "https://doi.org/10.1016/j.bbrc.2005.04.095" @default.
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