ArticleScientific reports2018
BST-2 promotes survival in circulation and pulmonary metastatic seeding of breast cancer cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
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- Emerging Oncogenic and Immunoregulatory Roles of BST2 in Human Cancers.Biomedicines · 2026Review
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- BST2 and DIRAS3 Drive Immune Evasion and Tumor Progression in High-Grade Glioma.International journal of molecular sciences · 2025Article
- Vascular smooth muscle cell plasticity in the tumor microenvironment.Cancer communications (London, England) · 2025Article
- Pan-Cancer Analysis of BST2 Expression, Prognostic Significance, and Immune Correlations.Cancer management and research · 2025Article
- The Role of Bone Marrow Stromal Cell Antigen 2 (BST2) in the Migration of Dendritic Cells to Lymph Nodes.International journal of molecular sciences · 2024Article
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- Bone marrow stromal cell antigen 2: Tumor biology, signaling pathway and therapeutic targeting (Review).Oncology reports · 2024Review
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- ALTEN: A High-Fidelity Primary Tissue-Engineering Platform to Assess Cellular Responses Ex Vivo.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- The genomic architecture of metastasis in breast cancer: focus on mechanistic aspects, signalling pathways and therapeutic strategies.Medical oncology (Northwood, London, England) · 2021Review
- Total ginsenosides induce autophagic cell death in cervical cancer cells accompanied by downregulation of bone marrow stromal antigen-2.Experimental and therapeutic medicine · 2021Article
- Transcriptomic profiling of three-dimensional cholangiocyte spheroids long term exposed to repetitive Clonorchis sinensis excretory-secretory products.Parasites & vectors · 2021Article
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Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Bone marrow stromal antigen 2 (BST-2) mediates various facets of cancer progression and metastasis. Here, we show that BST-2 is linked to poor survival in invasive breast cancer patients as its expression positively correlates with disease severity. However, the mechanisms that drive the pro-metastatic functions of BST-2 are not fully understood. Correlation of BST-2 expression and tumor aggressiveness was analyzed in human tissue samples. Migration, invasion, and competitive experimental metastasis assays were used to measure the cellular responses after silencing BST-2 expression. Using a mouse model of breast cancer, we show that BST-2 promotes metastasis independent of the primary tumor. Additional experiments show that suppression of BST-2 renders non-adherent cancer cells non-viable by sensitizing cells to anoikis. Embedment of cancer cells in basement membrane matrix reveals that silencing BTS-2 expression inhibits invadopodia formation, extracellular matrix degradation, and subsequent cell invasion. Competitive experimental pulmonary metastasis shows that silencing BST-2 reduces the numbers of viable circulating tumor cells (CTCs) and decreases the efficiency of lung colonization. Our data define a previously unknown function for BST-2 in the i) formation of invadopodia, ii) degradation of extracellular matrix, and iii) protection of CTCs from hemodynamic stress. We believe that physical (tractional forces) and biochemical (ECM type/composition) cues may control BST-2's role in cell survival and invadopodia formation. Collectively, our findings highlight BST-2 as a key factor that allows cancer cells to invade, survive in circulation, and at the metastatic site.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.