Abstract
The expression of decay-accelerating factor (DAF), a complement regulatory protein, is enhanced in colorectal cancer. In this study, to elucidate mechanisms for enhanced DAF expression, we studied the effects of growth factors on DAF expression in HT-29 human colonic cancer cells. Cells were treated with epidermal growth factor (EGF), insulin-like growth factor-I, platelet-derived growth factor, and transforming growth factor-β. DAF protein expression and mRNA expression were determined with enzyme immunoassay and Northern blot analysis. The signaling pathways that target DAF expression in response to growth factor stimulation were characterized by using various inhibitors of the signal transduction pathway. EGF induced significant increases in DAF protein and mRNA expression in HT-29 cells; the other growth factors had a weak effect or no effect. The EGF-induced DAF expression was inhibited by mitogen-activated protein (MAP) kinase kinase inhibitor PD 98059 but not by phosphatidylinositol-3 kinase inhibitor, phospholipase Cy inhibitor, or protein kinase C inhibitor. When we analyzed the phosphorylation state of the MAP kinase by immunoblot analysis, phosphorylated p44/p42 MAP kinase was detected in EGF-stimulated HT-29 cells, and the addition of PD 98059 abrogated the phosphorylation. These results indicate that EGF regulates DAF expression in HT-29 cells via the signaling pathway that depends on the activation of MAP kinase.
| Original language | English |
|---|---|
| Pages (from-to) | 186-192 |
| Number of pages | 7 |
| Journal | Journal of Laboratory and Clinical Medicine |
| Volume | 138 |
| Issue number | 3 |
| DOIs | |
| Publication status | Published - 2001 |
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ASJC Scopus subject areas
- Medicine(all)
- Pathology and Forensic Medicine
Cite this
Epidermal growth factor induces expression of decay-accelerating factor in human colonic cancer cells via the mitogen-activated protein kinase pathway. / Takeuchi, Kazuaki; Mizuno, Motowo; Uesu, Tokurou; Nasu, Junichirou; Kawada, Mikihiro; Hori, Shinitirou; Okada, Hiroyuki; Endo, Yuichi; Fujita, Teizo; Tsuji, Takao.
In: Journal of Laboratory and Clinical Medicine, Vol. 138, No. 3, 2001, p. 186-192.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Epidermal growth factor induces expression of decay-accelerating factor in human colonic cancer cells via the mitogen-activated protein kinase pathway
AU - Takeuchi, Kazuaki
AU - Mizuno, Motowo
AU - Uesu, Tokurou
AU - Nasu, Junichirou
AU - Kawada, Mikihiro
AU - Hori, Shinitirou
AU - Okada, Hiroyuki
AU - Endo, Yuichi
AU - Fujita, Teizo
AU - Tsuji, Takao
PY - 2001
Y1 - 2001
N2 - The expression of decay-accelerating factor (DAF), a complement regulatory protein, is enhanced in colorectal cancer. In this study, to elucidate mechanisms for enhanced DAF expression, we studied the effects of growth factors on DAF expression in HT-29 human colonic cancer cells. Cells were treated with epidermal growth factor (EGF), insulin-like growth factor-I, platelet-derived growth factor, and transforming growth factor-β. DAF protein expression and mRNA expression were determined with enzyme immunoassay and Northern blot analysis. The signaling pathways that target DAF expression in response to growth factor stimulation were characterized by using various inhibitors of the signal transduction pathway. EGF induced significant increases in DAF protein and mRNA expression in HT-29 cells; the other growth factors had a weak effect or no effect. The EGF-induced DAF expression was inhibited by mitogen-activated protein (MAP) kinase kinase inhibitor PD 98059 but not by phosphatidylinositol-3 kinase inhibitor, phospholipase Cy inhibitor, or protein kinase C inhibitor. When we analyzed the phosphorylation state of the MAP kinase by immunoblot analysis, phosphorylated p44/p42 MAP kinase was detected in EGF-stimulated HT-29 cells, and the addition of PD 98059 abrogated the phosphorylation. These results indicate that EGF regulates DAF expression in HT-29 cells via the signaling pathway that depends on the activation of MAP kinase.
AB - The expression of decay-accelerating factor (DAF), a complement regulatory protein, is enhanced in colorectal cancer. In this study, to elucidate mechanisms for enhanced DAF expression, we studied the effects of growth factors on DAF expression in HT-29 human colonic cancer cells. Cells were treated with epidermal growth factor (EGF), insulin-like growth factor-I, platelet-derived growth factor, and transforming growth factor-β. DAF protein expression and mRNA expression were determined with enzyme immunoassay and Northern blot analysis. The signaling pathways that target DAF expression in response to growth factor stimulation were characterized by using various inhibitors of the signal transduction pathway. EGF induced significant increases in DAF protein and mRNA expression in HT-29 cells; the other growth factors had a weak effect or no effect. The EGF-induced DAF expression was inhibited by mitogen-activated protein (MAP) kinase kinase inhibitor PD 98059 but not by phosphatidylinositol-3 kinase inhibitor, phospholipase Cy inhibitor, or protein kinase C inhibitor. When we analyzed the phosphorylation state of the MAP kinase by immunoblot analysis, phosphorylated p44/p42 MAP kinase was detected in EGF-stimulated HT-29 cells, and the addition of PD 98059 abrogated the phosphorylation. These results indicate that EGF regulates DAF expression in HT-29 cells via the signaling pathway that depends on the activation of MAP kinase.
UR - http://www.scopus.com/inward/record.url?scp=17944372233&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=17944372233&partnerID=8YFLogxK
U2 - 10.1067/mlc.2001.117405
DO - 10.1067/mlc.2001.117405
M3 - Article
C2 - 11528371
AN - SCOPUS:17944372233
VL - 138
SP - 186
EP - 192
JO - Translational Research
JF - Translational Research
SN - 1931-5244
IS - 3
ER -