MiR-301a-3p Promotes Triple-Negative Breast Cancer Progression via PTEN Suppression in Tumor Cells and the

Hai Yun Lin1,2, Guang Yan Li1,2, Wen Long Liang1

  • 1Department of Breast Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.

World Journal of Oncology
|November 10, 2025
PubMed
Abstract

Insights

MicroRNA-301a-3p promotes triple-negative breast cancer (TNBC) by interacting with adipose-derived stem cells (ADSCs). This interaction suppresses PTEN, activating pathways that drive tumor growth and making miR-301a-3p a potential therapeutic target for TNBC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Triple-negative breast cancer (TNBC) is an aggressive subtype with significant mortality.
  • Adipose-derived stem cells (ADSCs) and microRNAs (miRNAs) are key players in the tumor microenvironment (TME).
  • The specific role of the miR-301a-3p/PTEN axis in TNBC progression remains unclear.

Purpose of the Study:

  • To investigate the role of miR-301a-3p and its target PTEN in TNBC.
  • To elucidate the mechanism by which miR-301a-3p influences TNBC progression in the TME.
  • To explore the potential of the miR-301a-3p/PTEN axis as a therapeutic target for TNBC.

Main Methods:

  • Comparative analysis of PTEN expression in TNBC tissues versus normal tissues.
  • Luciferase reporter assays and functional cell experiments to assess molecular mechanisms.
  • Co-culture models with ADSCs and in vivo tumor models to evaluate TME interactions and tumor growth.

Main Results:

  • MiR-301a-3p was found to be upregulated in TNBC and directly inhibits PTEN expression.
  • MiR-301a-3p promotes TNBC cell malignancy and is transported via exosomes to ADSCs.
  • This exosome-mediated transfer suppresses PTEN in ADSCs, activating the PI3K/AKT pathway and increasing VEGFA, thereby promoting tumor growth in vivo.

Conclusions:

  • MiR-301a-3p drives TNBC progression through exosome-mediated communication with ADSCs, establishing a PTEN/PI3K/AKT/VEGFA signaling axis.
  • MiR-301a-3p represents a promising therapeutic target and a novel biomarker for TNBC treatment.

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