MiR-301a-3p Promotes Triple-Negative Breast Cancer Progression via PTEN Suppression in Tumor Cells and the Microenvironment.
Lin HY., Li GY., Liang WL., Wang Y., Fu BY., Du QG.
Animal Study, published in World J Oncol (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- World J Oncol (2025)
- Country
- Canada
- Reported sample size
- —
- Source database
- PubMed
- PMID
- 41208846
- PMCID
- PMC12591227
- DOI
- 10.14740/wjon2670
Abstract (original English)
Background Triple-negative breast cancer (TNBC), the most aggressive breast cancer subtype, poses a severe threat to women's health. Adipose-derived stem cells (ADSCs) and microRNAs (miRNAs) critically influence tumor progression within the tumor microenvironment (TME), but the role of the miR-301a-3p/PTEN axis in TNBC requires elucidation. Methods PTEN expression and effects were assessed by comparing clinical TNBC tissues with adjacent normal tissues. Mechanisms were investigated using integrated dataset analysis, luciferase reporter assays, functional cell experiments (assessing malignant phenotypes), co-culture models with ADSCs, and in vivo tumor models. Molecular expression (PTEN, vascular endothelial growth factor A (VEGFA)) and pathway activity (phosphoinositide 3-kinase (PI3K)/AKT) were evaluated. Results MiR-301a-3p was upregulated in TNBC and directly bound PTEN's 3'-UTR to suppress its expression. Functionally, miR-301a-3p enhanced tumor cell malignancy. Tumor cell-derived exosomes transported miR-301a-3p to ADSCs in the TME, suppressing PTEN, activating the PI3K/AKT pathway, and upregulating VEGFA secretion. In vivo , modulating miR-301a-3p levels significantly altered tumor growth, PTEN expression, and VEGFA production in tumor and peritumoral tissues. Conclusion MiR-301a-3p drives TNBC progression via exosome-mediated crosstalk with ADSCs, forming a PTEN/PI3K/AKT
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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