PT  - JOURNAL ARTICLE
AU  - SUZUKI, RYOKO
AU  - GOPALRAO, RAJESH KATARE
AU  - MAEDA, HIRONORI
AU  - RAO, PARIJATHA
AU  - YAMAMOTO, MORIO
AU  - XING, YUTONG
AU  - MIZOBUCHI, SHUNJI
AU  - SASAGURI, SHIRO
TI  - MCI-186 Inhibits Tumor Growth Through Suppression of EGFR Phosphorylation and Cell Cycle Arrest
DP  - 2005 Mar 01
TA  - Anticancer Research
PG  - 1131--1138
VI  - 25
IP  - 2A
4099  - http://ar.iiarjournals.org/content/25/2A/1131.short
4100  - http://ar.iiarjournals.org/content/25/2A/1131.full
SO  - Anticancer Res2005 Mar 01; 25
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