Antiproliferative effect of gold(I) compound auranofin through inhibition of STAT3 and telomerase activity in MDA-MB 231 human breast cancer cells

• Main Authors: Nam-Hoon Kim, Hyo Jung Park, Mi-Kyung Oh, In-Sook Kim
• Format: Article
• Language: English
• Published: Korean Society for Biochemistry and Molecular Biology 2013-01-01
• Series: BMB Reports
• Subjects: Antiproliferation; Auranofin; MDA-MB 231 cells; STAT3; Telomerase
• Online Access: http://bmbreports.org/jbmb/pdf.php?data=MTMwOTI2MTZAcGRmX3JhaW50cmFjZV9sZWV5c0AlNUI0Ni0xJTVEMTMwMTI5MjEyMl8lMjgwNTktMDY0JTI5Qk1CXzEyLTEyMy5wZGY=

Signal transducer and activator of transcription 3 (STAT3) andtelomerase are considered attractive targets for anticancertherapy. The in vitro anticancer activity of the gold(I) compoundauranofin was investigated using MDA-MB 231 human breastcancer cells, in which STAT3 is constitutively active. In cellculture, auranofin inhibited growth in a dose-dependent manner,and N-acetyl-L-cysteine (NAC), a scavenger of reactive oxygenspecies (ROS), markedly blocked the effect of auranofin.Incorporation of 5-bromo-2’-deoxyuridine into DNA andanchorage-independent cell growth on soft agar were decreasedby auranofin treatment. STAT3 phosphorylation and telomeraseactivity were also attenuated in cells exposed to auranofin, butNAC pretreatment restored STAT3 phosphorylation andtelomerase activity in these cells. These findings indicate thatauranofin exerts in vitro antitumor effects in MDA-MB 231 cellsand its activity involves inhibition of STAT3 and telomerase.Thus, auranofin shows potential as a novel anticancer drug thattargets STAT3 and telomerase. [BMB Reports 2013; 46(1): 59-64]