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  3. Hypoxic Bmsc-derived Exosomal Mir-210-3p Promotes Progression Of Triple-negative Breast Cancer Cells Via Nfix-wnt/β-catenin Signaling Axis.
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  3. Hypoxic Bmsc-derived Exosomal Mir-210-3p Promotes Progression Of Triple-negative Breast Cancer Cells Via Nfix-wnt/β-catenin Signaling Axis.

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Hypoxic BMSC-derived exosomal miR-210-3p promotes progression of triple-negative breast cancer cells via

Meng Wang1, Yi Zheng1,2, Qian Hao1

  • 1The Comprehensive Breast Care Center, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.

Journal of Translational Medicine
|January 9, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

Hypoxic bone marrow mesenchymal stem cells (BMSCs) release exosomes containing miR-210-3p, which promotes triple-negative breast cancer (TNBC) progression by targeting NFIX and activating Wnt/β-catenin signaling.

Keywords:
ExosomesHypoxiaNFIX-Wnt/β-catenin axisTriple-negative breast cancermiR-210-3p

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Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Bone marrow mesenchymal stem cells (BMSCs) are key players in the tumor microenvironment (TME).
  • Hypoxic conditions within the TME influence BMSC migration and exosome function.
  • Exosomes mediate intercellular communication, impacting cancer progression.

Purpose of the Study:

  • To investigate the role of exosomal microRNA (miRNA) from hypoxic BMSCs in triple-negative breast cancer (TNBC).
  • To elucidate the specific molecular mechanisms involved in this communication.
  • To assess the clinical relevance of these findings in TNBC patients.

Main Methods:

  • Exosome isolation (ultracentrifugation) and characterization (SEM, NTA, western blot).
  • Bioinformatic analysis for miRNA and mRNA target prediction.
  • In vitro assays for cell proliferation, apoptosis, migration, and invasion.
  • In vivo studies using tumor xenograft models.
  • Analysis of exosomal miRNA in patient serum.

    • Main Results:

    • Hypoxic BMSC-derived exosomes promote TNBC proliferation, migration, invasion, and epithelial-mesenchymal transition while inhibiting apoptosis.
    • miR-210-3p is significantly upregulated in exosomes from hypoxic BMSCs.
    • miR-210-3p targets NFIX in TNBC cells, activating the Wnt/β-Catenin signaling pathway.
    • In vivo deletion of miR-210-3p attenuated TNBC progression.
    • Elevated serum exosomal miR-210-3p in TNBC patients correlates with disease progression.

    Conclusions:

    • Hypoxic BMSC-derived exosomal miR-210-3p promotes TNBC progression.
    • This promotion occurs through the NFIX-Wnt/β-catenin signaling axis.
    • Exosomal miR-210-3p represents a potential therapeutic target and biomarker for TNBC.