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

被引:25
|
作者
Yi, Eun Hee [1 ]
Yoo, Hyouna [3 ]
Noh, Kum Hee [1 ]
Han, Songhee [1 ]
Lee, Haeri [1 ]
Lee, Jin-Ku [1 ]
Won, Cheolhee [1 ,6 ]
Kim, Byung-Hak [1 ,6 ]
Kim, Myoung-Hwan [4 ,5 ,6 ]
Cho, Chung-Hyun [1 ,2 ]
Ye, Sang-kyu [1 ,2 ,6 ]
机构
[1] Seoul Natl Univ, Coll Med, Dept Pharmacol & Biomed Sci, Seoul 110799, South Korea
[2] Seoul Natl Univ, Coll Med, Ischem Hypox Dis Inst, Seoul 110799, South Korea
[3] Yonsei Univ, Med Ctr, ISU ABXIS Co Ltd, Seoul 120752, South Korea
[4] Seoul Natl Univ, Coll Med, Dept Physiol, Seoul 110799, South Korea
[5] Seoul Natl Univ, Bundang Hosp, Songnam 463707, Gyeonggi, South Korea
[6] Seoul Natl Univ, Coll Med, Neuroimmune Informat Storage Network Res Ctr, Seoul 110799, South Korea
基金
新加坡国家研究基金会;
关键词
BST-2; Tamoxifen resistance; STAT3; Metastasis; CARCINOMA XENOGRAFT; MELANOMA-CELLS; EXPRESSION; METASTASIS; GROWTH; STAT3; GENE; IFN;
D O I
10.1016/j.bbrc.2013.05.043
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:685 / 690
页数:6
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