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Updated: Jan 11, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
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.
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/VEGFA signaling axis. It represents a promising therapeutic target and novel biomarker with significant clinical value for TNBC treatment.
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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