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BST-2 is a potential activator of invasion and migration in tamoxifen-resistant breast cancer cells

Cited 21 time in Web of Science Cited 19 time in Scopus

Yi, Eun Hee; Yoo, Hyouna; Noh, Kum Hee; Han, Songhee; Lee, Haeri; Lee, Jin-Ku; Won, Cheolhee; Kim, Byung-Hak; Kim, Myoung-Hwan; Cho, Chung-Hyun; Ye, Sang-kyu

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Academic Press
Biochemical and Biophysical Research Communications, Vol.435 No.4, pp.685-690
Bone marrow stromal cell antigen 2 (BST-2) is a type II transmembrane protein that is known to be a therapeutic target in several types of cancer. However, despite its clinical importance, the roles of BST-2 expression have remained elusive. Here, we found that BST-2 expression is up-regulated in tamoxifen-resistant MCF-7 human breast cancer (TRM-7) cells, resulting in enhanced invasiveness and migration. Matrigel and wound healing assays also showed that overexpression of BST-2 increased invasion and migration in MCF-7 cells, whereas invasion and migration were decreased by the silencing of BST-2 in TRM-7 cells. In addition, B16F10 cells expressing BST-2 showed increased metastatic melanoma nodule growth in a lung metastasis mouse model. Furthermore, BST-2 expression and promoter activity were regulated by activated signal transducer and activator of transcription 3 (STAT3). Taken together, our results indicate that BST-2 is an important factor in the invasiveness and motility of tamoxifen-resistant breast cancer cells, and that its expression and activity are regulated by activated STAT3. Therefore, regulation of BST-2 is a potential therapeutic target for tamoxifen-resistant breast cancer. (C) 2013 Elsevier Inc. All rights reserved.
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  • Department of Medicine
Research Area Translational Medicine, 3D drug screening, Cancer Organoid, Precision Oncologuy


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