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Author Notes:

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

There is no potential conflict of interest to disclose.

Subjects:

Research Funding:

This study was financially supported by a Research Grant from NIH NCI (1R01CA109366) to HS.

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Pharmacology & Pharmacy
  • Breast cancer
  • HDAC inhibitor
  • SAHA
  • MiR-200c
  • CRKL
  • SUBEROYLANILIDE HYDROXAMIC ACID
  • HISTONE-DEACETYLASE INHIBITORS
  • CHRONIC MYELOGENOUS LEUKEMIA
  • MESENCHYMAL TRANSITION
  • MICRORNA
  • EXPRESSION
  • ZEB1
  • METASTASIS
  • VORINOSTAT
  • PROMOTES

HDAC inhibitor suppresses proliferation and invasion of breast cancer cells through regulation of miR-200c targeting CRKL

Tools:

Journal Title:

Biochemical Pharmacology

Volume:

Volume 147

Publisher:

, Pages 30-37

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Although histone deacetylase (HDAC) inhibitors have been shown to effectively induce the inhibition of proliferation and migration in breast cancer, the anticancer mechanism remains poorly understood. Our studies show that miR-200c was significantly downregulated in breast cancer cell lines compared to normal cell lines and inversely correlated with the levels of class IIa HDACs and CRKL. HDAC inhibitors and the ectopic expression of miR-200c as tumor suppressors inhibited the proliferation, invasion, and migration of breast cancer cells by downregulating CRKL. These results indicate that the anticancer mechanism of HDAC inhibitor was realized partially by regulating miR-200c via CRKL targeting. Our findings suggest that the HDAC-miR200c-CRKL signaling axis could be a novel diagnostic marker and potential therapeutic target in breast cancer.

Copyright information:

© 2017 Elsevier Inc.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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