Bone marrow stromal antigen 2 expressed in cancer cells promotes mammary tumor growth and metastasis

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• 作者：Wadie D Mahauad-Fernandez (1) (2)
  Kris A DeMali (2) (3)
  Alicia K Olivier (4) (5)
  Chioma M Okeoma (1) (2)
  
  1. Department of Microbiology ; Carver College of Medicine ; University of Iowa ; 51 Newton Road ; Iowa City ; IA ; 52242-1109 ; USA
  2. Interdisciplinary Graduate Program in Molecular and Cellular Biology (MCB) ; University of Iowa ; 500 Newton Road ; Iowa City ; IA ; 52242-1109 ; USA
  3. Department of Biochemistry ; Carver College of Medicine ; University of Iowa ; 51 Newton Road ; Iowa City ; IA ; 52242-1109 ; USA
  4. Department of Pathology ; Carver College of Medicine ; University of Iowa ; 51 Newton Road ; Iowa City ; IA ; 52242-1109 ; USA
  5. Department of Pathobiology and Population Medicine ; College of Veterinary Medicine ; Mississippi State University ; 240 Wise Center Drive ; Starkville ; MS ; 39762-6100 ; USA
  
• 刊名：Breast Cancer Research
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：16
• 期：6
• 全文大小：4,092 KB
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• 刊物主题：Cancer Research; Oncology;
• 出版者：BioMed Central
• ISSN：1465-5411

文摘

Introduction Several innate immunity genes are overexpressed in human cancers and their roles remain controversial. Bone marrow stromal antigen 2 (BST-2) is one such gene whose role in cancer is not clear. BST-2 is a unique innate immunity gene with both antiviral and pro-tumor functions and therefore can serve as a paradigm for understanding the roles of other innate immunity genes in cancers. Methods Meta-analysis of tumors from breast cancer patients obtained from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) datasets were evaluated for levels of BST-2 expression and for tumor aggressiveness. In vivo, we examined the effect of knockdown of BST-2 in two different murine carcinoma cells on tumor growth, metastasis, and survival. In vitro, we assessed the effect of carcinoma cell BST-2 knockdown and/or overexpression on adhesion, anchorage-independent growth, migration, and invasion. Results BST-2 in breast tumors and mammary cancer cells is a strong predictor of tumor size, tumor aggressiveness, and host survival. In humans, BST-2 mRNA is elevated in metastatic and invasive breast tumors. In mice, orthotopic implantation of mammary tumor cells lacking BST-2 increased tumor latency, decreased primary tumor growth, reduced metastases to distal organs, and prolonged host survival. Furthermore, we found that the cellular basis for the role of BST-2 in promoting tumorigenesis include BST-2-directed enhancement in cancer cell adhesion, anchorage-independency, migration, and invasion. Conclusions BST-2 contributes to the emergence of neoplasia and malignant progression of breast cancer. Thus, BST-2 may (1) serve as a biomarker for aggressive breast cancers, and (2) be a novel target for breast cancer therapeutics.