Drug Design, Development and Therapy (Feb 2016)

Calycosin inhibits migration and invasion through modulation of transforming growth factor beta-mediated mesenchymal properties in U87 and U251 cells

  • Nie XH,
  • Ou-yang J,
  • Xing Y,
  • Li DY,
  • Liu RE,
  • Xu RX

Journal volume & issue
Vol. 2016, no. Issue 1
pp. 767 – 779

Abstract

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Xiao-hu Nie,1,* Jia Ou-yang,2,* Ying Xing,3 Dan-yan Li,4 Ru-en Liu,5 Ru-xiang Xu6 1Department of Neurosurgery, Huzhou Central Hospital, Huzhou, Zhejiang, 2Nanchang University Medical College, Nanchang, Jiangxi, 3Department of Gastroenterology, The 98th Hospital of Nanjing Military Command, Huzhou, Zhejiang, 4Spleen & Stomach Institute, Guangzhou University of Traditional Chinese Medicine, Guangzhou, Guangdong, 5Department of Neurosurgery, China–Japan Friendship Hospital, Beijing, 6Bayi Brain Hospital, The Military General Hospital of Beijing PLA, Beijing, People’s Republic of China *These authors contributed equally to this work Abstract: In this study, we investigated the potential anticancer effects of calycosin against human glioblastoma cells, including the impacts on cell proliferation, apoptosis, and cell cycle distribution. We further studied its inhibitory activity on migration and invasion in U87 and U251 cells. Furthermore, transforming growth factor beta-mediated reductions of mesenchymal-associated genes/activators, matrix metalloproteinases-2, and -9 were detected in this process. Administration of calycosin in a glioblastoma xenograft model showed that calycosin could not only reduce tumor volume but also suppress transforming growth factor beta as well as its downstream molecules. These results revealed calycosin as a potential antitumor agent in human glioblastoma. Keywords: calycosin, migration, invasion, epithelial–mesenchymal transition (EMT), matrix metalloproteinases (MMPs), glioblastoma

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