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MEK/ERK-mediated proliferation is negatively regulated by P38 map kinase in the human pancreatic cancer cell line, PANC-1.

Abstract：

:Pancreatic carcinoma is characterized by a poor prognosis and lack of response to conventional therapy. The regulatory mechanisms for the rapid proliferation of pancreatic cancer cells and the particular aggressiveness of this cancer are still not fully understood. In mammalian cells, three MAPK families including ERK, JNK, and P38 MAPK have been characterized. ERK is known to play an important role in regulating pancreatic cancer cell proliferation. However, the role of P38 kinase in pancreatic cancer cell proliferation and its relationship with ERK are unclear. Using the specific P38 inhibitor, SB203580 we found that blockade of P38 MAP kinase significantly enhanced proliferation of the pancreatic cancer cell line, PANC-1 cell, in a concentration-dependent manner. In parallel with the stimulation of proliferation, blockade of P38 MAP kinase markedly induced MEK and ERK1/2 phosphorylation, indicating an interaction between MEK/ERK and P38 MAP kinase signaling. Clearly, the interaction between these kinase pathways does not involve transcription and translation because MEK/ERK was activated immediately upon SB203580 treatment. Furthermore, inhibition of the MEK/ERK cascade using the MEK inhibitor, PD098059 abolished SB203580-induced PANC-1 cell proliferation. From these results, we conclude that a MEK/ERK and P38 MAP kinase interaction is important for pancreatic cancer cell proliferation. Breaking the balance between these two signaling pathways will modify pancreatic cancer cell proliferation.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Ding XZ,Adrian TE

doi

10.1006/bbrc.2001.4595

subject

Has Abstract

pub_date

2001-03-30 00:00:00

pages

447-53

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(01)94595-4

journal_volume

282

pub_type

杂志文章

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