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BST-2 is a potential activator of invasion and migration in tamoxifen-resistant breast cancer cells
- 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
- Biochemical and biophysical research communications 2013 v.435 pp. 685-690
- animal models, antigens, bone marrow, breast neoplasms, humans, melanoma, metastasis, neoplasm cells, signal transduction, tissue repair, transcription factors
- 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.