Abstract
Gastrin has the ability to stimulate cell growth in some colorectal cancer cells and
some of these cells also express gastrin/CCKB receptors, suggesting that gastrin and
its autocrine loop are involved in their proliferation. We previously reported that
oncogenic ras induced gastrin gene expression in colon cancer cells. The aim of this
study was to investigate whether oncogenic ras also induces gastrin/CCKB receptor
gene expression. A transiently transfected activated ras vector stimulated gastrin/CCKB
receptor transcriptional activities in both Colo320HSR and LoVo cells, but these ras-increased
activities were inhibited by a specific MEK inhibitor, PD98059. An RPA demonstrated
that activated ras increased endogenous gastrin/CCKB receptor mRNA levels and PD98059
decreased them in LoVo cells. These findings suggest that oncogenic ras induces gastrin/CCKB
receptor gene expression through some intracellular signaling pathways, including
MEK, in colon cancer cell lines.
Keywords:
APC (adenomatous polyposis coli), bp (base pair), CCKB (cholecystokinin B), DMSO (dimethylsulfoxide), EDTA (ethylenediaminetetraacetic acid), ERK (extracellular signal–regulated kinase), FCS (fetal calf serum), GAPDH (glyceraldehyde phosphate dehydrogenase), gly-gastrin (glycine-extended gastrin), MAPK (mitogen-activated protein kinase), MEK (MAPK/ERK kinase), mRNA (messenger RNA), RLU (relative light unit), RPA (ribonuclease-protection assay), RT-PCR (reverse transcription–polymerase chain reaction), SDS (sodium dodecyl sulfate), SEM (standard error of the mean), TCF-4 (T-cell factor-4)To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
December 10,
2002
Received in revised form:
December 3,
2002
Received:
April 8,
2002
Identification
Copyright
© 2003 Elsevier Science Inc. Published by Elsevier Inc. All rights reserved.