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, C.; Kim, Byung Hak; Kim, Myoung-Hwan; Cho, Chung Hyun; Ye, Sang kyu

doi:10.1016/j.bbrc.2013.05.043

Cited by 26 publications

(27 citation statements)

References 16 publications

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“…Although the attributes of BST-2 that orchestrate its tumorigenic behavior 1, 2, 3, 4 are not well understood, the tumorigenic functions of BST-2 in mouse models of breast cancer are consistent with human clinical data. 3 Various cellular mechanisms, including, cell to cell adhesion, anchorage-independent growth, migration and invasion have been associated with BST-2-mediated promotion of cancer.…”

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confidence: 61%

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Cysteine-linked dimerization of BST-2 confers anoikis resistance to breast cancer cells by negating proapoptotic activities to promote tumor cell survival and growth

Mahauad‐Fernandez

Okeoma

2017

Cell Death Dis

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Almost all breast tumors express the antiviral protein BST-2 with 67%, 25% and 8.2% containing high, medium or low levels of BST-2, respectively. Breast tumor cells and tissues that contain elevated levels of BST-2 are highly aggressive. Suppression of BST-2 expression reprograms tumorigenic properties of cancer cells and diminishes cancer cell aggressiveness. Using structure/function studies, we report that dimerization of BST-2 through cysteine residues located in the BST-2 extracellular domain (ECD), leads to anoikis resistance and cell survival through proteasome-mediated degradation of BIM—a key proapoptotic factor. Importantly, BST-2 dimerization promotes tumor growth in preclinical breast cancer models in vitro and in vivo. Furthermore, we demonstrate that restoration of the ECD cysteine residues is sufficient to rescue cell survival and tumor growth via a previously unreported pathway—BST-2/GRB2/ERK/BIM/Cas3. These findings suggest that disruption of BST-2 dimerization offers a potential therapeutic approach for breast cancer.

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mentioning

confidence: 61%

“…3 Various cellular mechanisms, including, cell to cell adhesion, anchorage-independent growth, migration and invasion have been associated with BST-2-mediated promotion of cancer. 1, 2, 3, 4 …”

mentioning

confidence: 99%

Cysteine-linked dimerization of BST-2 confers anoikis resistance to breast cancer cells by negating proapoptotic activities to promote tumor cell survival and growth

Mahauad‐Fernandez

Okeoma

2017

Cell Death Dis

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“…Cai et al also reported BST-2 protein expression to be associated with breast cancer bone metastasis in a smaller cohort (n=50) of breast samples (22). Experimental data, based on cell lines and in vivo models, have hinted that BST-2 was involved in increased proliferation and reduced apoptosis (23), as well as increased migration, invasion and metastasis (21,22,24). The data we are presenting imply that the role of BST-2 in metastasis is specific to patients with ER-negative tumours, and may be further enhanced by sLe x expression.…”

Section: Discussionmentioning

confidence: 98%

Two E-selectin ligands, BST-2 and LGALS3BP, predict metastasis and poor survival of ER-negative breast cancer

Woodman¹,

Pinder²,

Tajadura³

et al. 2016

International Journal of Oncology

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Abstract. Distant metastases account for the majority of cancer-related deaths in breast cancer. The rate and site of metastasis differ between estrogen receptor (ER)-negative and ER-positive tumours, and metastatic fate can be very diverse even within the ER-negative group. Characterisation of new pro-metastatic markers may help to identify patients with higher risk and improve their care accordingly. Selectin ligands aberrantly expressed by cancer cells promote metastasis by enabling interaction between circulating tumour cells and endothelial cells in distant organs. These ligands consist in carbohydrate molecules, such as sialyl-Lewis x antigen (sLe x ), borne by glycoproteins or glycolipids on the cancer cell surface. We have previously demonstrated that the molecular scaffold presenting sLe x to selectins (e.g. glycolipid vs. glycoproteins) was crucial for these interactions to occur. Moreover, we reported that detection of sLe x alone in breast carcinomas was only of limited prognostic value. However, since sLe x was found to be carried by several glycoproteins in cancer cells, we hypothesized that the combination of the carbohydrate with its carriers could be more relevant than each marker independently. In this study, we addressed this question by analysing sLe x expression together with two glycoproteins (BST-2 and LGALS3BP), shown to interact with E-selectin in a carbohydrate-dependent manner, in a cohort of 249 invasive breast cancers. We found both glycoproteins to be associated with distant metastasis risk and poorer survival. Importantly, concomitant high expression of BST-2 with sLe x defined a subgroup of patients with ER-negative tumours displaying higher risks of liver and brain metastasis and a 3-fold decreased survival rate.

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“…BST2 knockdown reduced cell proliferation and invasive activity of RCC cells. A previous study reported that BST2 expression is up-regulated in tamoxifen-resistant MCF-7 human breast cancer cells, resulting in enhanced invasiveness and migration (24). Although the precise biological functions of BST2 in tumourigenesis is not yet fully understood, another study showed that BST2 can enhance tumour cell invasion and metastasis through signal transducer and activator of transcription 3 (STAT3)/BST2/interleukin-6 pathway (24).…”

Section: Discussionmentioning

confidence: 99%

The Expression of BTS-2 Enhances Cell Growth and Invasiveness in Renal Cell Carcinoma

Pham

Oue

Yamamoto

et al. 2017

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

Cited by 26 publications

References 16 publications

Cysteine-linked dimerization of BST-2 confers anoikis resistance to breast cancer cells by negating proapoptotic activities to promote tumor cell survival and growth

Cysteine-linked dimerization of BST-2 confers anoikis resistance to breast cancer cells by negating proapoptotic activities to promote tumor cell survival and growth

Two E-selectin ligands, BST-2 and LGALS3BP, predict metastasis and poor survival of ER-negative breast cancer

The Expression of BTS-2 Enhances Cell Growth and Invasiveness in Renal Cell Carcinoma

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