scholarly journals Effect of hGC-MSCs from human gastric cancer tissue on cell proliferation, invasion and epithelial-mesenchymal transition in tumor tissue of gastric cancer tumor-bearing mice

2016 ◽  
Vol 9 (8) ◽  
pp. 796-800 ◽  
Author(s):  
Lin Song ◽  
Xin Zhou ◽  
Hong-Jun Jia ◽  
Mei Du ◽  
Jin-Ling Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Tumor Tissue ◽  
Epithelial Mesenchymal Transition ◽  
Gastric Cancer Tissue ◽  
Cancer Tissue ◽  
Human Gastric Cancer ◽  
Mesenchymal Transition ◽  
Tumor Bearing ◽  
Cancer Tumor

Effect of Long Non-Coding RNA Plasmacytoma Variant Translocation 1 (PVT1) on the Regulation of SRY (Sex Determining Region Y)-Box 2 (SOX2) in Gastric Cancer

2020 ◽  
Vol 10 (8) ◽  
pp. 1213-1218
Author(s):  
Jinhe Zhou ◽  
Lingli Hu ◽  
Jianbin Huang ◽  
Zhiqing Ye
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Gastric Cancer Cell ◽  
Caspase 3 ◽  
Gastric Cancer Tissue ◽  
Tetrazolium Salt ◽  
Cancer Tissue ◽  
Mesenchymal Transition

The pathogenesis of gastric cancer (GC) is unclear, which has brought major problems in the diagnosis and treatment. LncRNAs is involved in the regulation of tumorigenesis and development. LncRNA PVT1 is abnormally expressed in various tumors, such as liver cancer and ovarian cancer. However, its role and mechanism in GC have not been clarified. The gastric cancer tissue and adjacent tissues were collected for measuring LncRNA PVT1 level by Real-time PCR. The gastric cancer cell line SGC-7901 was cultured in vitro and divided into control group, scramble group, and PVT1 siRNA group. The tetrazolium salt (MTT) colorimetric assay was to analyze cell proliferation. Caspase 3 activity was tested to assess cell apoptosis. Transwell chamber assay was adopted to evaluated cell invasion. Western Blot was for measuring the epithelial-mesenchymal transition (EMT) molecular proteins and SOX2. Significantly upregulated LncRNA PVT1 was found in gastric cancer tissue (P < 0 05) which was associated tumor differentiation and stage and lymph node metastasis (P < 0 05). LncRNA PVT1 siRNA transfection in SGC-7901 significantly downregulated LncRNA PVT1 expression, inhibited tumor cell proliferation, enhanced Caspase 3 activity, restrained gastric cancer cell invasion, elevated E-cadherin level, reduced Vimentin expression, and declined SOX2 expression (P < 0 05). LncRNA PVT1 is upregulated in gastric cancer and related to the clinical pathology. Downregulation of LncRNA PVT1 inhibits cell proliferation, invasion, and EMT by regulating SOX2, thereby delaying the progression of gastric cancer.

Research on Function of Exosome of miR-328-3p Secreted by Bone Marrow Mesenchymal Stem Cells (BMSCs) on Restraining the Gastric Cancer Through Being Down-Regulated with Trefoil Factor 3

2022 ◽  
Vol 12 (4) ◽  
pp. 854-861
Author(s):  
Jing Li ◽  
Bo Xie ◽  
Hu Wang ◽  
Chengsong Chen ◽  
Chengwu Pan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Bone Marrow ◽  
Cell Proliferation ◽  
Gastric Cancer Tissue ◽  
Cancer Tissue ◽  
Trefoil Factor ◽  
Trefoil Factor 3 ◽  
Marrow Mesenchymal Stem Cells ◽  
Made In ◽  
E Cadherin

Certain progress has been made in the therapeutic method against gastric cancer such as surgical operation combined with chemotherapy and radiation therapy in recent years. But the therapeutic efficacy and prognosis on gastric cancer was still not satisfactory. The function of exosome of miR-328–3p secreted by bone marrow stromal cells (BMSCs) on restraining the gastric cancer was studied in the present study. The BMSCs with highly-expressed miR-328-3p was established. The exosome in cell supernatant was collected. The exosome of BMSCs and MSCs with highlyexpressed miR-328-3p was added into SGC-7901 cells followed by analysis of miR-328-3p level by Real-time PCR and TFF3 (Trefoil Factor 3) level in exosome by Western blot, cell proliferation, expression of E-cadherin, Vimentin and Caspase-3. miR-328-39 expression was reduced and TFF3 was elevated in gastric cancer tissue (P < 0.05). miR-328-3p was upregulated and TFF3 was downregulated after addition of BMSCs exosomes along with increased cell proliferation and reduced E-cadherin and Caspase3 expression (P < 0.05). In conclusion, exosome of BMSCs could be regulated by miR-328-3p and TFF3 expression is restrained so as to regulate the biological behaviors of gastric cancer cell.

lncRNA NEAT1 Inhibits Proliferation, Invasion and Epithelial-mesenchymal Transition of Gastric Cancer Cells by Regulating MiR-129-5p/PBX3 Axis

2020 ◽  
Author(s):  
Hanshu Ji ◽  
Xiaoyu Zhang
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Luciferase Reporter ◽  
Reporter Assay ◽  
Gastric Cancer Cells ◽  
Mesenchymal Transition ◽  
Lncrna Neat1 ◽  
Dual Luciferase Reporter Assay

Abstract Purpose: lncRNA NEAT1 has been reported as a tumor-promoting gene in a variety of tumors, but few studies have explored its role and mechanism in gastric cancer. In the face of increasing incidence of gastric cancer, how to improve the diagnostic accuracy and therapeutic effect of gastric cancer is a major clinical problem. Therefore, we studied the effect and mechanism of lncRNA NEAT1 on the proliferation, invasion and epithelial-mesenchymal transition of gastric cancer cells. To inquiry into the effect of lncRNA NEAT1 on the proliferation, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer (GC) cells by regulating miR-129-5p/PBX3 axis. Methods: Totally 63 GC diagnosed and treated in our hospital were selected as the study subjects, whose paired GC tissues and pericarcinomatous tissues were collected as the study specimens after obtaining their consent. QRT-PCR was employed to detect the NEAT1 expression in tissues and cells to analyze the relationship between NEAT1 and clinicopathological data of GC patients. In addition, stable and transient overexpression and inhibition vectors were established and transfected into GC cells HCG-27 and MKN-45. CCK-8, traswell, and flow cytometry were employed to evaluate the proliferation, invasion, and apoptosis of transfected cells. The correlation of miR-129-5p between PBX3 and NEAT1 was assessed using dual luciferase reporter assay, while that between NEAT1 and miR-129-5p was assessed by RNA-binding protein immunoprecipitation (RIP) . Western blot was applied for the detection of apoptosis and EMT related proteins.Results: NEAT1 was overexpressed in GC patients and had a high diagnostic value. The expression of NEAT1 was related to the pathological stage, differentiation degree, tumor size and lymph node metastasis of patients with GC. Down-regulated NEAT1 brought decreased cell proliferation, invasion and EMT, and increased apoptosis. According to dual luciferase reporter assay, NEAT1 could target miR-129-5p, while in turn miR-129-5p could target PBX3. Functional analysis exhibited that miR-129-5p overexpression inhibited PBX3 in GC cells, affecting cell proliferation, invasion, EMT and apoptosis, and rescue experiments demonstrated that these effects were eliminated by up-regulating NEAT1 expression.Conclusion: Inhibition of NEAT1 could mediate miR-129-5p/PBX3 axis to promote apoptosis of GC cells, and reduce cell proliferation, invasion and EMT.

scholarly journals Hyperglycemia promotes Snail-induced epithelial–mesenchymal transition of gastric cancer via activating ENO1 expression

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Xin Xu ◽  
Bang Chen ◽  
Shaopu Zhu ◽  
Jiawei Zhang ◽  
Xiaobo He ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Transforming Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
The Cancer Genome Atlas ◽  
Migration And Invasion ◽  
Gastrointestinal Malignancies ◽  
Mesenchymal Transition

Abstract Background Gastric cancer (GC) is one of the most common gastrointestinal malignancies worldwide. Emerging evidence indicates that hyperglycemia promotes tumor progression, especially the processes of migration, invasion and epithelial–mesenchymal transition (EMT). However, the underlying mechanisms of GC remain unclear. Method Data from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases were used to detect the expression of glycolysis-related enzymes and EMT-related transcription factors. Small interfering RNA (siRNA) transfection was performed to decrease ENO1 expression. Immunohistochemistry (IHC), Western blot and qRT-PCR analyses were used to measure gene expression at the protein or mRNA level. CCK-8, wound-healing and Transwell assays were used to assess cell proliferation, migration and invasion. Results Among the glycolysis-related genes, ENO1 was the most significantly upregulated in GC, and its overexpression was correlated with poor prognosis. Hyperglycemia enhanced GC cell proliferation, migration and invasion. ENO1 expression was also upregulated with increasing glucose concentrations. Moreover, decreased ENO1 expression partially reversed the effect of high glucose on the GC malignant phenotype. Snail-induced EMT was promoted by hyperglycemia, and suppressed by ENO1 silencing. Moreover, ENO1 knockdown inhibited the activation of transforming growth factor β (TGF-β) signaling pathway in GC. Conclusions Our results indicated that hyperglycemia induced ENO1 expression to trigger Snail-induced EMT via the TGF-β/Smad signaling pathway in GC.

scholarly journals High-Throughput Screening Identifies miR-451 as a Pleiotropic Modulator That Suppresses Gastric Cancer Metastasis

2016 ◽  
Vol 22 (2) ◽  
pp. 136-143 ◽  
Author(s):  
Wendao You ◽  
Liang Xu ◽  
Xing Zhang ◽  
Huan Zou ◽  
Dongtao Shi ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Migration ◽  
High Throughput Screening ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Human Gastric Cancer ◽  
Mesenchymal Transition ◽  
Therapeutic Uses ◽  
Human Carcinomas ◽  
Insight Into

MicroRNAs (miRNAs) are globally dysregulated in human carcinomas. However, the specific miRNAs that mediate gastric cancer metastasis have not been identified. We identified 100 miRNAs that are dysregulated in gastric cancer and used a self-assembled cell microarray method to systematically evaluate their capacity to regulate cell migration. MiR-451, which is down-regulated in human gastric cancer samples, potently modulated multiple metastatic phenotypes including cell migration, invasion, proliferation, and epithelial-mesenchymal transition. These effects were achieved via down-regulation of the miR-451 target gene, ERK2. These findings provide new insight into the physiological effects of and potential therapeutic uses for miRNAs in gastric cancer.

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