scholarly journals The role of mmu-miR-155-5p-NF-κB signaling in the education of bone marrow-derived mesenchymal stem cells by gastric cancer cells

2018 ◽  
Vol 7 (3) ◽  
pp. 856-868 ◽  
Author(s):  
Mei Wang ◽  
Fang Yang ◽  
Rong Qiu ◽  
Mengchu Zhu ◽  
Huiling Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Gastric Cancer Cells

The Regulatory Effect of miR-126-3p Exosomes Derived from Bone Marrow Mesenchymal Stem Cells (BMSCs) Targeting Endothelial Cell Specific Molecule 1 on Gastric Cancer

2021 ◽  
Vol 11 (12) ◽  
pp. 2415-2420
Author(s):  
Sujuan Wu ◽  
Jinyan Wang ◽  
Tao Niu
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Gene Reporter Assay ◽  
Marrow Mesenchymal Stem Cells ◽  
Other Substances

Exosomes can transmit microRNAs (miRNAs) and other substances between different cells. Bone marrow mesenchymal stem cells (BMSCs) can migrate to tumor sites. They are related to a variety of tumors, but the role of miR-126-3p exosomes derived from BMSCs in gastric cancer has not been elucidated. miR-126-3p overexpressing BMSCs were established and cell supernatant exosomes were collected followed by measuring miR-126-3p level by PCR, ESM1 expression by western blot, targeting relationship by dual luciferase gene reporter assay along with analysis of cell proliferation, invasion and apoptosis. The addition of BMSCs exosomes to gastric cancer cells reduced the miR-126-3p level, promoted ESM1 expression, and worsened the biological behaviors of tumor cells. miR-126-3p-overexpressed BMSCs exosomes promoted miR-126-3p expression, resulting in the decrease of ESM1 expression and inhibiting the further deterioration. In conclusion, BMSCs can inhibit the increase of miR-126-3p expression and ESM1 to inhibit the deterioration of biological behaviors of gastric cancer cells.

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.

scholarly journals Wnt5a‐Ror2 signaling in mesenchymal stem cells promotes proliferation of gastric cancer cells by activating CXCL16–CXCR6 axis

2016 ◽  
Vol 107 (3) ◽  
pp. 290-297 ◽  
Author(s):  
Gosuke Takiguchi ◽  
Michiru Nishita ◽  
Kana Kurita ◽  
Yoshihiro Kakeji ◽  
Yasuhiro Minami
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Gastric Cancer Cells

scholarly journals G6PD-NF-κB-HGF Signal in Gastric Cancer-Associated Mesenchymal Stem Cells Promotes the Proliferation and Metastasis of Gastric Cancer Cells by Upregulating the Expression of HK2

2021 ◽  
Vol 11 ◽  
Author(s):  
Bin Chen ◽  
Tuo Cai ◽  
Chao Huang ◽  
Xueyan Zang ◽  
Li Sun ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Underlying Mechanism ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gastric Cancer Cells ◽  
Proliferation And Metastasis

Background: Tumor-associated stromal cells have been widely recognized for their tumor-promoting capability involving paracrine signaling. However, the underlying mechanism and the effects of the molecules in the glycolysis pathway in gastric cancer-associated mesenchymal stem cells (GCMSCs) and gastric cancer cells on tumor progression remain unclear.Methods: The expression of hepatocyte growth factor (HGF) in GCMSCs and bone marrow mesenchymal stem cells (BMMSCs) was detected by enzyme-linked immunosorbent assay (ELISA). The effect of HGF derived from GCMSCs on the proliferation, metastasis, and HK2 expression of gastric cancer cells was evaluated in vitro and in vivo. The effects of G6PD on the production of HGF in mesenchymal stem cells (MSCs) were analyzed by immunoblotting.Results: HGF derived from GCMSCs promoted glycolysis, proliferation, and metastasis of gastric cancer by upregulating c-Myc-HK2 signal. The progression of the disease induced by GCMSCs decelerated in the absence of HK2. The expression of G6PD activated NF-κB signaling and stimulated the production of HGF in GCMSCs. Blocking HGF derived from GCMSCs decreased proliferation, metastasis, and angiogenesis of gastric cancer cells in vivo.Conclusions: GCMSCs highly expressed G6PD and facilitated the progression of gastric cancer through the G6PD-NF-κB-HGF axis coordinates. Blocking HGF derived from GCMSCs is a potential new therapeutic target for the treatment of gastric cancer.

scholarly journals microRNA-375 released from extracellular vesicles of bone marrow mesenchymal stem cells exerts anti-oncogenic effects against cervical cancer

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Feng Ding ◽  
Jinhua Liu ◽  
Xiaofei Zhang
Keyword(s):  
Cervical Cancer ◽  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Cancer Cells ◽  
Extracellular Vesicles ◽  
Cervical Cancer Cells ◽  
Marrow Mesenchymal Stem Cells

Abstract Background Cervical cancer is the most prevalent gynecological malignancies accompanied by high mortality, where finding a more effective therapeutic option for cervical cancer is necessary. The inhibitory role of microRNAs (miRNAs) derived from the extracellular vesicles (EVs) of the bone marrow mesenchymal stem cells (BMSCs) was analyzed in cervical cancer. Methods Expression of miR-375 was examined by RT-qPCR in cervical cancer cell lines. The targeting relation between miR-375 and maternal embryonic leucine zipper kinase (MELK) was predicted by bioinformatics analysis and verified by dual-luciferase reporter gene assay. Isolated BMSCs were transfected with lentivirus-mediated vectors, followed by EV extraction. The morphology of EVs was then identified using a NanoSight particle size analyzer and transmission electron microscope (TEM). The biological properties of cervical cancer cells were evaluated using Transwell, EdU, and TUNEL assays, respectively. Xenograft tumors in nude mice were observed to assess cervical tumorigenesis in vivo. Results Low expression of miR-375 and high expression of MELK were detected in cervical cancer samples. MELK was identified as the target gene of miR-375, which was negatively correlated with miR-375 levels. Overexpression of miR-375 suppressed proliferation, migration, and invasion of cervical cancer cells, but enhanced cell apoptosis by cooperating with downregulated MELK expression. miR-375 transferred from BMSC-derived EVs exerted the same effects on cell biological activities. Xenograft assays in vivo proved that miR-375 from BMSC-derived EVs inhibited tumor growth. Conclusion The present study highlighted the role of miR-375 from BMSC-derived EVs in suppressing the progression of cervical cancer, which may contribute to the discovery of novel potential biomarkers for cervical cancer therapy.

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