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Tamoxifen differentially regulates miR-29b-1 and miR-29a expression depending on endocrine-sensitivity in breast

Penn Muluhngwi1, Abirami Krishna1, Stephany L Vittitow1

  • 1Department of Biochemistry & Molecular Genetics, Center for Genetics and Molecular Medicine, University of Louisville School of Medicine, Louisville, KY 40292, USA.

Cancer Letters
|December 18, 2016
PubMed

Insights

MicroRNAs miR-29a and miR-29b-1 show tumor suppressor activity in tamoxifen-resistant breast cancer cells. However, these microRNAs do not appear to play a role in mediating tamoxifen resistance.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • Endocrine resistance to tamoxifen (TAM) affects approximately 40% of breast cancer patients.
  • The role of microRNAs in the development of endocrine resistance remains unclear.
  • Previous studies indicated differential regulation of miR-29a and miR-29b-1 by TAM in sensitive versus resistant breast cancer cells.

Purpose of the Study:

  • To investigate the mechanism of differential miR-29a/b-1 regulation by TAM.
  • To determine the functional role of miR-29a/b-1 in tamoxifen-resistant breast cancer cells.
  • To explore the potential of miR-29a/b-1 in overcoming tamoxifen resistance.

Main Methods:

  • Analysis of miR-29a/b-1 regulation by TAM in MCF-7, LY2, and LCC9 cells.
  • Estrogen receptor alpha (ERα) knockdown studies.
  • Overexpression of miR-29a/b-1 and assessment of cell proliferation, migration, and colony formation.
  • Investigation of DICER1 regulation by miR-29a/b-1 and TAM.

Main Results:

  • ERα mediates TAM regulation of miR-29b-1/a transcription.
  • Overexpression of miR-29b-1/a reduced proliferation in all tested cell lines and inhibited migration and colony formation in LY2 cells.
  • TAM treatment reduced DICER1 in LY2 cells, and anti-miR-29 inhibition blocked this effect.
  • miR-29b-1/a did not sensitize resistant cells to TAM.

Conclusions:

  • miR-29b-1/a exhibits tumor suppressor activity in tamoxifen-resistant breast cancer cells.
  • miR-29b-1/a does not appear to mediate tamoxifen resistance.
  • ERα plays a key role in the tamoxifen-dependent regulation of miR-29b-1/a.
Keywords:
Breast cancerEndocrine-resistanceEstrogen receptorTamoxifenmiRNA-29amiRNA-29b-1

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