scholarly journals Tumor-Educated Neutrophils Activate Mesenchymal Stem Cells to Promote Gastric Cancer Growth and Metastasis

2020 ◽  
Vol 8 ◽  
Author(s):  
Jiahui Zhang ◽  
Cheng Ji ◽  
Wei Li ◽  
Zheying Mao ◽  
Yinghong Shi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cancer Growth

scholarly journals Activation of Mesenchymal Stem Cells by Macrophages Prompts Human Gastric Cancer Growth through NF-κB Pathway

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97569 ◽  
Author(s):  
Tingting Yang ◽  
Xu Zhang ◽  
Mei Wang ◽  
Jie Zhang ◽  
Feng Huang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cancer Growth ◽  
Human Gastric Cancer

scholarly journals Enhanced gastric cancer growth potential of mesenchymal stem cells derived from gastric cancer tissues educated by CD4+T cells

2017 ◽  
Vol 51 (2) ◽  
pp. e12399 ◽  
Author(s):  
Rongman Xu ◽  
Xiangdong Zhao ◽  
Yuanyuan Zhao ◽  
Bin Chen ◽  
Li Sun ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
T Cells ◽  
Mesenchymal Stem Cells ◽  
Cd4 T Cells ◽  
Growth Potential ◽  
Cancer Growth ◽  
Cancer Tissues

scholarly journals Human Bone Marrow Mesenchymal Stem Cells Promote Gastric Cancer Growth via Regulating c-Myc

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Bin Chen ◽  
Jing Yu ◽  
Qianqian Wang ◽  
Yuanyuan Zhao ◽  
Li Sun ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Clinical Application ◽  
Human Bone ◽  
Human Bone Marrow ◽  
Cancer Growth ◽  
Gastric Cancer Cells ◽  
Marrow Mesenchymal Stem Cells

The clinical application of human bone marrow mesenchymal stem cells (hBM-MSCs) has generated a great deal of interest because of their potential use in regenerative medicine and tissue engineering. However, safety concerns over hBM-MSCs limit their clinical application. In this study, we observed that hBM-MSC-conditioned medium (hBM-MSC-CM) promotes gastric cancer development via upregulation of c-Myc. Our results showed that c-Myc was upregulated in MGC-803 and BGC-823 cells after hBM-MSC-CM treatment. Moreover, we found that the c-Myc inhibitor JQ1 and c-Myc siRNA decreased the expression of c-Myc in hBM-MSC-CM-treated tumor cells in vitro. Additionally, hBM-MSC-CM enhanced the migration and glucose uptake of gastric cancer cells. In vivo studies showed that JQ1 inhibited hBM-MSC-CM-induced gastric cancer growth. These results indicated that hBM-MSC-CM induced gastric cancer growth via upregulation of c-Myc, which may be a potential risk factor and/or a therapeutic target for clinical applications.

scholarly journals Lymph node metastasis-derived gastric cancer cells educate bone marrow-derived mesenchymal stem cells via YAP signaling activation by exosomal Wnt5a

Oncogene ◽  
2021 ◽  
Vol 40 (12) ◽  
pp. 2296-2308
Author(s):  
Mei Wang ◽  
Xinxin Zhao ◽  
Rong Qiu ◽  
Zheng Gong ◽  
Feng Huang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Lymph Node ◽  
Lymph Node Metastasis ◽  
Metastatic Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Node Metastasis ◽  
Signaling Activation

AbstractLymph node metastasis (LNM), a common metastatic gastric-cancer (GC) route, is closely related to poor prognosis in GC patients. Bone marrow-derived mesenchymal stem cells (BM-MSCs) preferentially engraft at metastatic lesions. Whether BM-MSCs are specifically reprogrammed by LNM-derived GC cells (LNM-GCs) and incorporated into metastatic LN microenvironment to prompt GC malignant progression remains unknown. Herein, we found that LNM-GCs specifically educated BM-MSCs via secretory exosomes. Exosomal Wnt5a was identified as key protein mediating LNM-GCs education of BM-MSCs, which was verified by analysis of serum exosomes collected from GC patients with LNM. Wnt5a-enriched exosomes induced YAP dephosphorylation in BM-MSCs, whereas Wnt5a-deficient exosomes exerted the opposite effect. Inhibition of YAP signaling by verteporfin blocked LNM-GC exosome- and serum exosome-mediated reprogramming in BM-MSCs. Analysis of MSC-like cells obtained from metastatic LN tissues of GC patients (GLN-MSCs) confirmed that BM-MSCs incorporated into metastatic LN microenvironment, and that YAP activation participated in maintaining their tumor-promoting phenotype and function. Collectively, our results show that LNM-GCs specifically educated BM-MSCs via exosomal Wnt5a-elicited activation of YAP signaling. This study provides new insights into the mechanisms of LNM in GC and BM-MSC reprogramming, and will provide potential therapeutic targets and detection indicators for GC patients with LNM.

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