TY - JOUR
T1 - Thalidomide inhibits epidermal growth factor-induced cell growth in mouse and human monocytic leukemia cells via Ras inactivation
AU - Noman, Abu Shadat M.
AU - Koide, Naoki
AU - Khuda, Imtiaz I.E.
AU - Dagvadorj, Jargalsaikhan
AU - Tumurkhuu, Gantsetseg
AU - Naiki, Yoshikazu
AU - Komatsu, Takayuki
AU - Yoshida, Tomoaki
AU - Yokochi, Takashi
N1 - Funding Information:
This work was supported by in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan. We are grateful to Kazuko Takahashi and Akiko Morikawa for the technical assistance.
PY - 2008/10/3
Y1 - 2008/10/3
N2 - The effect of thalidomide on epidermal growth factor (EGF)-induced cell growth was examined. Thalidomide inhibited EGF-induced cell growth in mouse and human monocytic leukemia cells, RAW 264.7, U937 and THP-1. Thalidomide inhibited EGF-induced phosphorylation of extracellular signal regulated kinase (ERK) 1/2, but not p38 and stress-activated protein kinase (SAPK)/JNK. The phosphorylation of MEK1/2 and Raf at Ser 338 as the upstream molecules of ERK 1/2 was also prevented by thalidomide. Further, it inhibited EGF-induced Ras activation through preventing the transition to GTP-bound active Ras. Thalidomide inhibited the Ras activation induced by lipopolysaccharide (LPS) and vascular endothelial growth factor (VEGF) as well as EGF. There was no significant difference in the expression and function of EGF receptor between thalidomide-treated and non-treated cells. Therefore, thalidomide was suggested to inhibit EGF-induced cell growth via inactivation of Ras.
AB - The effect of thalidomide on epidermal growth factor (EGF)-induced cell growth was examined. Thalidomide inhibited EGF-induced cell growth in mouse and human monocytic leukemia cells, RAW 264.7, U937 and THP-1. Thalidomide inhibited EGF-induced phosphorylation of extracellular signal regulated kinase (ERK) 1/2, but not p38 and stress-activated protein kinase (SAPK)/JNK. The phosphorylation of MEK1/2 and Raf at Ser 338 as the upstream molecules of ERK 1/2 was also prevented by thalidomide. Further, it inhibited EGF-induced Ras activation through preventing the transition to GTP-bound active Ras. Thalidomide inhibited the Ras activation induced by lipopolysaccharide (LPS) and vascular endothelial growth factor (VEGF) as well as EGF. There was no significant difference in the expression and function of EGF receptor between thalidomide-treated and non-treated cells. Therefore, thalidomide was suggested to inhibit EGF-induced cell growth via inactivation of Ras.
UR - http://www.scopus.com/inward/record.url?scp=49449106486&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=49449106486&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2008.07.090
DO - 10.1016/j.bbrc.2008.07.090
M3 - Article
C2 - 18662673
AN - SCOPUS:49449106486
SN - 0006-291X
VL - 374
SP - 683
EP - 687
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 4
ER -