Human umbilical cord wharton's jelly mesenchymal stem cells do not transform to tumor-associated fibroblasts in the presence of breast and ovarian cancer cells unlike bone marrow mesenchymal stem cells

2012 ◽  
Vol 113 (6) ◽  
pp. 1886-1895 ◽  
Author(s):  
Arjunan Subramanian ◽  
Gan Shu-Uin ◽  
Ngo Kae-Siang ◽  
Kalamegam Gauthaman ◽  
Arijit Biswas ◽  
...  
2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Xiaohe Luo ◽  
Shan Huang ◽  
Ningning He ◽  
Chen Liu ◽  
Yanan Chen ◽  
...  

To ensure the safety of clinical applications of MSCs, thorough understanding of their impacts on tumor initiation and progression is essential. Here, to further explore the complex dialog between MSCs and tumor cells, umbilical cord-derived mesenchymal stem cells (UC-MSCs) were employed to be cocultured with either breast or ovarian cancer cells. Though having no obvious influence on proliferation or apoptosis, UC-MSCs exerted intense stem cell-like properties promoting effects on both cancer models. Cocultured cancer cells showed enriched side population, enhanced sphere formation ability, and upregulated pluripotency-associated stem cell markers. Human cytokine array and real-time PCR revealed a panel of MSC-derived prostemness cytokines CCL2, CXCL1, IL-8, and IL-6 which were induced upon coculturing. We further revealed IL-1β, a well-characterized proinflammatory cytokine, to be the inducer of these prostemness cytokines, which was generated from inflammatory UC-MSCs in an autocrine manner. Additionally, with introduction of IL-1RA (an IL-1 receptor antagonist) into the coculturing system, the stem cell-like characteristics promoting effects of inflammatory UC-MSCs were partially blocked. Taken together, these findings suggest that transduced inflammatory MSCs work as a major source of IL-1β in tumor microenvironment and initiate the formation of prostemness niche via regulating their secretome in an IL-1β-dependent manner.


2022 ◽  
Vol 12 (2) ◽  
pp. 273-278
Author(s):  
Daqing Jiang ◽  
Xianxin Xie ◽  
Cong Wang ◽  
Weijie Li ◽  
Jianjun He

Our study intends to assess the relationship between exosomes derived from bone marrow mesenchymal stem cells (BMSC-exo) and breast cancer. BMSC-exo were isolated and characterized by transmission electron microscopy. After transfection of BMSCs with miR-204 inhibitor, breast cancer cells were incubated with BMSC-exo followed by analysis of cell proliferation by CCK-8 assay, cell apoptosis by flow cytometry, and expression of apoptosis-related protein and NF-κB signaling by western blot. The co-culture of BMSC-exo with breast cancer cells enhanced miR-204 transcription, inhibited cell proliferation and induced apoptosis. Further, BMSC-exo accelerated apoptosis as demonstrated by the increased level of Bax and casepase-3 and decreased Bcl-2 expression, as well as reduced NF-κB signaling activity. But knockdown of miR-204 abolished the effect of BMSC-exo on apoptosis and proliferation with NF-κB signaling activation. In conclusion, miR-204 from BMSC-exo restrains growth of breast cancer cell and might be a novel target for treating breast cancer.


2017 ◽  
Vol 210 ◽  
pp. 64-75 ◽  
Author(s):  
Hanaa S.E. Mousa ◽  
Sally M. Shalaby ◽  
Zienab A. Gouda ◽  
Fayza E. Ahmed ◽  
Aisha A. El-Khodary

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Dequan Li ◽  
Cong Wang ◽  
Chuang Chi ◽  
Yuanyuan Wang ◽  
Jing Zhao ◽  
...  

Background. Systemic inflammatory response syndrome (SIRS) accompanied by trauma can lead to multiple organ dysfunction syndrome (MODS) and even death. Early inhibition of the inflammation is necessary for damage control. Bone marrow mesenchymal stem cells (BMSCs), as a novel therapy modality, have been shown to reduce inflammatory responses in human and animal models.Methods. In this study, we used Western blot, quantitative PCR, and enzyme-linked immunosorbent assay (ELISA) to assess the activity of BMSCs to suppress the inflammation induced by lipopolysaccharide (LPS) in human umbilical cord endothelial cells (HUVECs) and alveolar macrophages.Results. Our results demonstrated that LPS caused an inflammatory response in alveolar macrophages and HUVECs, increased permeability of HUVEC, upregulated expression of toll-like receptor (TLR) 2, TLR4, phosphorylated p65, downregulated release of IL10, and promoted release of TNF-αin both cells. Coculture with BMSCs attenuated all of these activities induced by LPS in the two tested cell types.Conclusions. Together, our results demonstrate that BMSCs dosage dependently attenuates the inflammation damage of alveolar macrophages and HUVECs induced by LPS.


2009 ◽  
Vol 52 (10) ◽  
pp. 1753-1761 ◽  
Author(s):  
Mahmoud Aghaee-afshar ◽  
Mohammad Rezazadehkermani ◽  
Alireza Asadi ◽  
Reza Malekpour-afshar ◽  
Armita Shahesmaeili ◽  
...  

2015 ◽  
Vol 51 ◽  
pp. S19-S20
Author(s):  
M. Gosset ◽  
C. Geyl ◽  
M. Mirshahi ◽  
M. Maleki ◽  
A. Rafii ◽  
...  

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