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Author Notes:

To whom Correspondence should be addressed: Dr. Zhongxing Liang, zliang@emory.edu or Dr. Hyunsuk Shim, hshim@emory.edu

The authors declare that they have no conflict of interest.

Subject:

Research Funding:

This study was financially supported by the Department of Defense Breast Cancer Program Concept Award (BC052118) to ZL as well as a Research Grant from NIH NCI (1R01CA165306) to HS. The authors thank Jessica Paulishen for proof-reading.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Oncology
  • MicroRNA
  • Breast cancer
  • Metastasis
  • CXCR4
  • CELL LINES
  • TUMOR
  • TARGETS
  • CLUSTER
  • GROWTH
  • GENE
  • ANGIOGENESIS
  • MIR-302-367
  • REPRESSION
  • THERAPY

Inhibition of breast cancer metastasis with microRNA-302a by downregulation of CXCR4 expression

Tools:

Journal Title:

Breast Cancer Research and Treatment

Volume:

Volume 146, Number 3

Publisher:

, Pages 535-542

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Metastasis remains a main cause of mortality from breast cancer and an unresolved issue. The purpose of this study is to investigate the role of miR-302a in the development of breast cancer metastasis mediated by CXCR4, a critical regulator of metastasis, and to identify miR-302a as an effective therapeutic agent for therapy and prevention of breast cancer metastasis. Our studies show that miR-302a expression levels were downregulated in metastatic breast cancer cells and tumor tissues. Additionally, the expression levels of miR-302a were inversely correlated with CXCR4 levels. More promisingly, miR-302a inhibited the invasion and metastasis of breast cancer cells in vitro and in vivo and reduced the expression of CXCR4. Our findings demonstrated that the repression of miR-302a levels contributes to breast cancer metastasis and restoration of miR-302a baseline expression inhibits the invasion and metastasis of breast cancer cells. These data suggest that miR-302a mimics are potential therapeutic agents for breast cancer metastasis.

Copyright information:

© 2014 Springer Science+Business Media.

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