Exosomes Derived from miR-143-Overexpressing MSCs Inhibit Cell Migration and Invasion in Human Prostate Cancer by Downregulating TFF3
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Updated: Jan 18, 2026
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Yuanyuan Che1, Xu Shi1, Yunpeng Shi2
1Clinical Laboratory, The First Hospital of Jilin University, Changchun 130000, P.R. China.
Abstract:
Exosomes are membrane-enclosed nanovesicles that shuttle active cargoes, such as mRNAs and microRNAs (miRNAs), between different cells. Mesenchymal stem cells (MSCs) are able to migrate to the tumor sites and exert complex functions over tumor progress. We investigated the effect of human bone marrow-derived MSC (BMSC)-derived exosomal miR-143 on prostate cancer. During the co-culture experiments, we disrupted exosome secretion by the inhibitor GW4869 and overexpressed exosomal miR-143 using miR-143 plasmid. miR-143 was involved in the progression of prostate cancer via trefoil factor 3 (TFF3). Moreover, miR-143 was downregulated while TFF3 was upregulated in prostate cancer cells and tissues, and miR-143 was found to specifically inhibit TFF3 expression. Human MSC-derived exosomes enriched miR-143 and transferred miR-143 to prostate cancer cells. Furthermore, elevated miR-143 or exosome-miR-143 or silencing TFF3 inhibited the expression of TFF3, proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP)-2, and MMP-9 and PC3 cell proliferation, migration, invasion, and tumor growth, whereas it promoted apoptosis. In conclusion, hMSC-derived exosomal miR-143 directly and negatively targets TFF3 to suppress prostate cancer.
Insights
Human mesenchymal stem cell (MSC)-derived exosomes carrying miR-143 suppress prostate cancer progression. These exosomes target trefoil factor 3 (TFF3), inhibiting cancer cell proliferation, migration, and tumor growth while promoting apoptosis.
Area of Science:
- Cell Biology
- Oncology
- Biochemistry
Background:
- Exosomes mediate intercellular communication by transferring molecules like microRNAs (miRNAs).
- Mesenchymal stem cells (MSCs) can target tumor sites and influence tumor progression.
- Prostate cancer is characterized by dysregulated gene expression, including miRNAs and target genes.
Purpose of the Study:
- To investigate the role of human bone marrow-derived MSC (BMSC)-derived exosomal miR-143 in prostate cancer.
- To determine the molecular mechanism by which exosomal miR-143 affects prostate cancer cells.
- To evaluate the therapeutic potential of MSC-derived exosomes in prostate cancer.
Main Methods:
- Co-culture experiments with prostate cancer cells and human MSCs.
- Inhibition of exosome secretion using GW4869.
- Overexpression of miR-143 in exosomes using miR-143 plasmid.
- Analysis of gene and protein expression (TFF3, PCNA, MMP-2, MMP-9).
- Assessment of cell proliferation, migration, invasion, and apoptosis.
Main Results:
- miR-143 was downregulated, and TFF3 was upregulated in prostate cancer tissues.
- MSC-derived exosomes enriched with miR-143 were transferred to prostate cancer cells.
- Exosomal miR-143 directly inhibited TFF3 expression.
- Elevated miR-143 or exosome-miR-143 suppressed PC3 cell proliferation, migration, invasion, and tumor growth.
- Increased apoptosis was observed in prostate cancer cells treated with exosomal miR-143.
Conclusions:
- Human MSC-derived exosomal miR-143 directly targets and suppresses TFF3 expression in prostate cancer.
- This mechanism inhibits prostate cancer progression by reducing proliferation, migration, invasion, and tumor growth.
- MSC-derived exosomes carrying miR-143 represent a potential therapeutic strategy for prostate cancer.
