MiR-16-5p inhibits breast cancer by reducing AKT3 to restrain NF-κB pathway

Liwei Ruan1, Xiaojun Qian2

  • 1Department of Breast and Thyroid Surgery, Shaoxing People's Hospital, Shaoxing Hospital of Zhejiang University, Shaoxing 312000.

Bioscience Reports
|August 7, 2019
PubMed

Insights

MicroRNA-16-5p (miR-16-5p) is downregulated in breast cancer, correlating with lower survival rates. Restoring miR-16-5p inhibits tumor growth by suppressing the NF-κB pathway and AKT3.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Breast cancer is a leading cause of death in women globally.
  • MicroRNAs (miRNAs) play crucial roles in regulating breast cancer cell behavior, including migration, proliferation, and apoptosis.
  • Understanding specific miRNA roles, like miR-16-5p, is vital for developing targeted therapies.

Purpose of the Study:

  • To investigate the expression levels of miR-16-5p in breast cancer.
  • To determine the functional impact of miR-16-5p on breast cancer cell pathogenesis, migration, proliferation, and apoptosis.
  • To elucidate the molecular mechanisms underlying miR-16-5p's role, particularly its relationship with AKT3 and the NF-κB pathway.

Main Methods:

  • Quantitative real-time PCR (qRT-PCR) for miR-16-5p expression analysis.
  • Cell proliferation (CCK8, EdU) and migration (Transwell) assays.
  • Dual-luciferase reporter assay, immunohistochemistry, and Western blotting to assess miR-16-5p, AKT3, and NF-κB pathway interactions.

Main Results:

  • miR-16-5p was significantly downregulated in breast cancer tissues and correlated with poorer patient survival.
  • Reduced miR-16-5p expression promoted breast cancer cell migration, proliferation, cell cycle progression, and inhibited apoptosis in vitro and in vivo.
  • miR-16-5p was found to inhibit the NF-κB pathway and decrease AKT3 expression, thereby suppressing breast cancer development.

Conclusions:

  • miR-16-5p acts as a tumor suppressor in breast cancer.
  • Low miR-16-5p expression contributes to breast cancer progression.
  • Targeting miR-16-5p or its downstream pathways (NF-κB, AKT3) may offer therapeutic strategies for breast cancer.

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