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Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further

Matteo Sibilano1, Valentina Tullio1, Gaspare Adorno2

  • 1Department of Experimental Medicine, University of Rome Tor Vergata, 00133 Rome, Italy.

International Journal of Molecular Sciences
|May 28, 2022
PubMed

Insights

Platelet microvesicles carrying miR-126-3p suppress breast cancer (BC) growth and invasion by targeting AKT2. High miR-126 and low AKT2 levels correlate with better BC patient prognosis, suggesting therapeutic potential.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Platelets and their released microvesicles (MVs) influence tumor biology.
  • Platelet MVs deliver microRNAs (miRNAs) that modulate cancer cell signaling.
  • Previous studies indicated anti-tumor effects of platelet MV-enriched miR-126 in breast cancer (BC).

Purpose of the Study:

  • To identify novel targets of miR-126-3p in breast cancer.
  • To investigate the role of AKT2 kinase as a direct target of miR-126-3p.
  • To evaluate the therapeutic potential of miR-126-3p delivery in BC.

Main Methods:

  • Bioinformatic analysis to predict miR-126-3p targets.
  • Luciferase assays to validate direct targeting of AKT2 by miR-126-3p.
  • Ectopic expression and MV-mediated delivery of miR-126-3p in BC cell lines (BT549 and MCF-7).
  • Assessment of proliferation and invasion assays.
  • Correlation analysis of miR-126 and AKT2 levels with patient prognosis.

Main Results:

  • AKT2 kinase was identified as a direct target of miR-126-3p.
  • Both ectopic and MV-mediated delivery of miR-126-3p downregulated AKT2 expression in BC cells.
  • Downregulation of AKT2 suppressed proliferation and invasion in triple-negative and Luminal A BC subtypes.
  • High miR-126 and low AKT2 levels were associated with favorable long-term prognosis in BC patients.

Conclusions:

  • miR-126-3p exerts tumor suppressor activity in breast cancer by targeting the PIK3/AKT signaling pathway, specifically via AKT2.
  • Platelet-derived MVs can deliver miR-126-3p to effectively downregulate AKT2 and inhibit BC progression.
  • Modulating platelet MV production and miR-126-3p delivery offers a potential strategy for multimodal BC therapy.
Keywords:
PIK3/AKT signalingbreast cancermiR-126microvesiclesplateletspolyunsaturated fatty acids

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