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Clinicopathological Analysis of miRNA Expression in Breast Cancer Tissues by Using miRNA In Situ Hybridization
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MiR-216b-5p inhibits cell proliferation in human breast cancer by down-regulating HDAC8 expression

Mohammad-Nazir Menbari1, Karim Rahimi2, Abbas Ahmadi3

  • 1Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran.

Life Sciences
|October 13, 2019
PubMed
Abstract

Insights

MicroRNA-216b-5p inhibits breast cancer progression by targeting histone deacetylase 8 (HDAC8). Lower miR-216b-5p levels correlate with advanced cancer, while its overexpression reduces proliferation and metastasis.

Area of Science:

  • Molecular oncology
  • Epigenetics
  • Cancer biology

Background:

  • Histone deacetylase 8 (HDAC8) is overexpressed in breast cancer, but its role in progression is unclear.
  • MicroRNAs (miRs) are key regulators in cancer, influencing oncogenes and tumor suppressors.
  • Understanding miR-216b-5p's interaction with HDAC8 is crucial for breast cancer research.

Purpose of the Study:

  • To investigate the role of miR-216b-5p in regulating HDAC8 expression.
  • To determine the impact of the miR-216b-5p/HDAC8 axis on breast cancer progression.
  • To elucidate the molecular mechanisms underlying HDAC8's function in breast cancer.

Main Methods:

  • Quantitative real-time PCR (qPCR) and Western blotting to assess miR-216b-5p and HDAC8 expression.
  • Cell proliferation, cell cycle, and colony formation assays to evaluate cancer progression.
  • Luciferase reporter assays and HDAC8 knockout vectors to confirm direct targeting and functional impact.

Main Results:

  • Breast cancer tissues and cell lines showed decreased miR-216b-5p and increased HDAC8 levels.
  • Reduced miR-216b-5p correlated with lymph node metastasis and larger tumor size.
  • miR-216b-5p overexpression inhibited proliferation and progression, directly down-regulating HDAC8.

Conclusions:

  • HDAC8 acts as an oncogene promoting breast cancer proliferation and progression.
  • miR-216b-5p suppresses these oncogenic functions by binding to the HDAC8 3'-UTR.
  • The miR-216b-5p/HDAC8 pathway represents a potential therapeutic target for breast cancer.
Keywords:
Breast cancerCancer progressionHDAC8miR-216b-5p

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