240 BAICALEIN BLOCKS AKT PHOSPHORYLATION AND INDUCES APOPTOSIS IN HUMAN RENAL CELL CARCINOMA 786-O AND 769-P CELLS

Abstract

You have accessJournal of UrologyKidney Cancer: Basic Research1 Apr 2011240 BAICALEIN BLOCKS AKT PHOSPHORYLATION AND INDUCES APOPTOSIS IN HUMAN RENAL CELL CARCINOMA 786-O AND 769-P CELLS Dong Zhang, Hongliang Li, Yan Xue, Weimin Gan, Tie Chong, Ziming Wang, and Dalin He Dong ZhangDong Zhang Xi'an, China, People's Republic of More articles by this author , Hongliang LiHongliang Li Xi'an, China, People's Republic of More articles by this author , Yan XueYan Xue Xi'an, China, People's Republic of More articles by this author , Weimin GanWeimin Gan Xi'an, China, People's Republic of More articles by this author , Tie ChongTie Chong Xi'an, China, People's Republic of More articles by this author , Ziming WangZiming Wang Xi'an, China, People's Republic of More articles by this author , and Dalin HeDalin He Xi'an, China, People's Republic of More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2011.02.309AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Baicalein (BE) is a main active ingredient of flavonoids derived from the root of Scutellaria baicalensis, which is widely used in traditional Chinese herbal medicine. Owing to its anti-inflammatory, anti-oxidant, and anti-cancer properties, BE was extensively used in therapeutic areas. Here, we investigated the potential role in inducing apoptosis of renal cell carcinoma (RCC) cells and possible underlying mechanisms. METHODS 786-O and 769-P cells were treated with BE and MTT was used to detect cell growth rate. Cell cycle and apoptosis were determined by flow cytometry after treatment of BE. Transwell assay was used to determine invasive potential. Western blot was used to detect Akt phosphorylation and apoptosis associated proteins. RESULTS In MTT assay, BE exhibited growth inhibition effects on both 786-O and 769-P cells in a time- and dose-dependent manner. Cell cycle assay demonstrated that cells were arrested at G1/S phase following BE treatment. In addition, BE induced a significant increased apoptosis of the two cells. Moreover, BE significantly inhibited invasive capability of both 786-O and 769-P cells in vitro. Mechanically, BE decreased the expression of Bcl-2, Bcl-xL, and survivin; it also stimulated cleaved caspase-3 and PARP. Furthermore, BE inhibited dose-dependent Akt phosphorylation. CONCLUSIONS Our data suggests that BE inhibits RCC 786-O and 769-P cells growth in a time- and dose-dependent manner and induces cellular apoptosis. In addition, BE leads to inhibition of invasion capability in RCC cells. The potential anti-cancer effect indicates BE can be a potential therapeutic strategy in RCC treatment. © 2011 by American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 185Issue 4SApril 2011Page: e97 Advertisement Copyright & Permissions© 2011 by American Urological Association Education and Research, Inc.MetricsAuthor Information Dong Zhang Xi'an, China, People's Republic of More articles by this author Hongliang Li Xi'an, China, People's Republic of More articles by this author Yan Xue Xi'an, China, People's Republic of More articles by this author Weimin Gan Xi'an, China, People's Republic of More articles by this author Tie Chong Xi'an, China, People's Republic of More articles by this author Ziming Wang Xi'an, China, People's Republic of More articles by this author Dalin He Xi'an, China, People's Republic of More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...