RT Journal Article
SR Electronic
T1 MCI-186 Inhibits Tumor Growth Through Suppression of EGFR Phosphorylation and Cell Cycle Arrest
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 1131
OP 1138
VO 25
IS 2A
A1 SUZUKI, RYOKO
A1 GOPALRAO, RAJESH KATARE
A1 MAEDA, HIRONORI
A1 RAO, PARIJATHA
A1 YAMAMOTO, MORIO
A1 XING, YUTONG
A1 MIZOBUCHI, SHUNJI
A1 SASAGURI, SHIRO
YR 2005
UL http://ar.iiarjournals.org/content/25/2A/1131.abstract
AB Background: It has been suggested that radicals stimulate tumor cell growth. We examined if the hydroxyl radical scavenger, 3-methyl-1-phenyl-2-pyrazolin-5-one (MCI-186), affects tumor growth in vitro. Materials and Methods: Human hepatocarcinoma HepG2, mesothelioma MSTO-211H, gastric carcinoma TMK-1 and breast carcinoma MCF-7 were used for cell proliferation assay. Cell cycle analysis was performed using propidium iodide for fluorescence activated cell sorter. By Western blotting, EGF receptor (EGFR) phosphorylation and EGFR expression were analyzed. Results: Growth inhibition was observed from 10 μM to 300 μM of MCI-186 in a dose-dependent manner. Cell cycle analysis revealed that MCI-186 arrested the cell cycle at the G0/G1-phase. MCI-186 inhibited EGF-stimulated cell growth. The phosphorylation level of EGFR was decreased by MCI-186, but the EGFR level was unchanged. Conclusion: From the data obtained, we suggest that tumor inhibition by MCI-186 was due, at least in part, to the modulation of EGFR signaling and cell cycle arrest. Copyright© 2005 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved