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Author Notes:

Corresponding author. Department of Radiology, Emory University, Atlanta, GA 30322, USA. zliang@emory.edu

We thank the Avon Tissue Bank for Translational Genomics Research at Grady Memorial Hospital for providing normal breast and breast tumor tissues.

The authors thank Ms. Jessica Paulishen and Ms. Amber Feng for proof-reading.

Subject:

Research Funding:

This study was financially supported by a Research Grant from NIH NCI (1R01CA165306).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Biochemistry & Molecular Biology
  • Biophysics
  • MicroRNA
  • Triple negative breast cancer
  • VEGF
  • Invasion
  • Angiogenesis
  • GROWTH-FACTOR VEGF
  • UP-REGULATION
  • LUNG-CANCER
  • EXPRESSION
  • SURVIVAL
  • CELLS
  • METASTASIS
  • CARCINOMA
  • PATHWAY
  • RADIORESISTANCE

Downregulation of microRNA-206 promotes invasion and angiogenesis of triple negative breast cancer

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Journal Title:

Biochemical and Biophysical Research Communications

Volume:

Volume 477, Number 3

Publisher:

, Pages 461-466

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Triple negative breast tumors don't respond to Tamoxifen and Herceptin, two of the most effective medications for treating breast cancer. Additionally, triple negative breast cancer (TNBC) intrinsically resists or will eventually acquire resistance to chemotherapy. The purpose of this study is to understand better the molecular basis of TNBC as well as develop new therapeutic strategies against it. Here, we analyzed miRNA-206 expression levels in breast cancer cell lines and tissues. In addition, we investigated whether miR-206 mimics inhibited TNBC tumor invasion and angiogenesis. The results showed that miR-206 was downregulated in TNBC compared to non-TNBC cell lines and tissues. Additionally, the decreased levels of miR-206 were inversely consistent with expression levels of VEGF. Furthermore, the forced expression of miR-206 in the mimic-transfected TNBC cells downregulated VEGF, MAPK3, and SOX9 expression levels. The miR-206 mimics inhibited TNBC breast cell invasion and angiogenesis. These findings demonstrate for the first time the involvement of miRNA-206 in TNBC invasion and angiogenesis and suggest that miR-206 may be an efficient agent for therapy of TNBC.

Copyright information:

© 2016 Elsevier Inc.

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