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EZH2 induces the expression of miR-1301 as a negative feedback control mechanism in triple negative breast cancer

Qiuju Wu1,2,3, Zekun Chen4, Guihua Zhang4

  • 1Fengxian District Center Hospital Graduate Student Training Base, Jinzhou Medical University, Shanghai, China.

Acta Biochimica Et Biophysica Sinica
|May 24, 2018
PubMed

Insights

EZH2 promotes miR-1301 expression in triple-negative breast cancer (TNBC). Overexpressing miR-1301 inhibits TNBC cell growth and tumor progression, revealing a negative feedback loop crucial for TNBC therapy development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • Triple-negative breast cancer (TNBC) lacks effective targeted therapies due to the absence of Estrogen Receptor alpha (ERα), Progesterone Receptor (PR), and Human Epidermal growth factor Receptor 2 (HER2) expression.
  • Identifying novel therapeutic targets and understanding regulatory mechanisms in TNBC are critical for improving patient outcomes.

Purpose of the Study:

  • To investigate the regulatory relationship between EZH2 and miR-1301 in TNBC.
  • To evaluate the therapeutic potential of modulating miR-1301 expression in TNBC.

Main Methods:

  • Lentivirus systems were employed to overexpress EZH2 and miR-1301 in TNBC cell lines (HCC1937, HCC1806).
  • Western blot, RT-qPCR, TCGA, and Kaplan Meier plotter databases were used for expression analysis.
  • Cell proliferation, migration, colony formation, and xenograft mouse models assessed miR-1301 function; dual luciferase reporter assay verified gene binding.

Main Results:

  • EZH2 was found to induce miR-1301 expression in TNBC cell lines.
  • Overexpression of miR-1301 significantly suppressed TNBC cell proliferation, migration, colony formation, and xenograft tumor growth.
  • miR-1301 directly inhibited EZH2 expression by binding to its 3'-untranslated region (3'-UTR), indicating a negative feedback mechanism.

Conclusions:

  • EZH2 positively regulates miR-1301 expression in TNBC, establishing a feedback loop where miR-1301 subsequently inhibits EZH2.
  • miR-1301 demonstrates significant tumor-suppressive functions in TNBC, highlighting its potential as a therapeutic target.
  • Understanding the EZH2-miR-1301 axis offers insights into TNBC pathogenesis and potential therapeutic strategies.

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