scholarly journals Expression of Angiogenin is inversely correlated to Progression of Gastric Tumors

2019 ◽  
pp. 120-136
Author(s):  
Yunxia Wu ◽  
Muntadher Al-sarraf ◽  
Huang Xiao-Tao ◽  
Zhang Zhi-qiang ◽  
Li Bin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Tumor Stage ◽  
Gastric Mucus ◽  
Adjacent Tissue ◽  
Glandular Cells ◽  
Differentiation Status ◽  
Cancer Tissues ◽  
Gastric Stem Cells

Objective: Angiogenin (ANG) is upregulated in a variety of cancers including those of prostate, cervix, pancreas, liver, oral cavity, skin, and etc., however, the role of ANG in gastric cancer has not been fully elucidated yet. We use tissue microarray (TMA) to examine ANG expression to investigate the role of ANG in the progression of gastric cancer. Method: Immunohistochemistry was used to evaluate ANG expression in TMA with 208 spots from 104 patients diagnosed with gastric cancer and the corresponding adjacent tissue. Results: In normal adjacent tissue, ANG was expressed mainly in cytoplasm at basal gland of the gastric mucus where gastric stem cells are reserved, and also sparsely expressed in the nucleus of gastric mucosal gland cells at isthmus where gastric stem cells are gathered. In cancer tissues, ANG was very sparsely expressed in the nucleus of gastric glandular cells. ANG expression in the cytoplasm was found to be significantly associated with pathological types (p<0.001) and malignancy (p<0.001). ANG expression in the nucleus was inversely correlated with malignancy (p=0.019), differentiation status (p< 0.001), and tumor stage (p= 0.048).Conclusion: ANG might play an important role in gastric cancer development.

scholarly journals SLCO4A1-AS1 Facilitates the Malignant Phenotype via miR-149-5p/STAT3 Axis in Gastric Cancer Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Qing Li ◽  
Dachuan Zhang ◽  
Hui Wang ◽  
Jun Xie ◽  
Lei Peng ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Organic Anion ◽  
Organic Anion Transporter ◽  
Gastric Cancer Cells ◽  
Anion Transporter ◽  
Transporter Family ◽  
Cancer Tissues ◽  
Development Of Gastric Cancer

Solute carrier organic anion transporter family member 4A1 (SLCO4A1-AS1), a newly discovered lncRNA, may exert effects in tumors. Since its role in gastric cancer remains obscure, we sought to explore the mechanism of SLCO4A1-AS1 in gastric cancer. The relationship among SLCO4A1-AS1, miR-149-5p, and STAT3 was detected by bioinformatics, dual luciferase analysis, and Pearson’s test, and the expressions of these genes were determined by quantitative real-time PCR and Western blot. Moreover, CCK-8, flow cytometry, wound healing assay, and Transwell analysis were performed to verify the function of SLCO4A1-AS1 in gastric cancer. Rescue experiments were used to detect the role of miR-149-5p. The expressions of SLCO4A1-AS1 and STAT3 were increased, while the expression of miR-149-5p was suppressed in gastric cancer tissues and cell lines. In addition, STAT3 expression was negatively correlated with miR-149-5p expression but was positively correlated with SLCO4A1-AS1 expression. Overexpression of SLCO4A1-AS1 promoted cell viability, migration, invasion, and STAT3 expression but suppressed apoptosis, while knockdown of SLCO4A1-AS1 had the opposite effect. SLCO4A1-AS1 bound to miR-149-5p and targeted STAT3. Moreover, miR-149-5p mimic inhibited the malignant development of gastric cancer cells and obviously reversed the function of SLCO4A1-AS1 overexpression. Our research reveals that abnormally increased SLCO4A1-AS1 expression may be an important molecular mechanism in the development of gastric cancer.

scholarly journals Core 1–derived mucin-type O-glycosylation protects against spontaneous gastritis and gastric cancer

2019 ◽  
Vol 217 (1) ◽  
Author(s):  
Fei Liu ◽  
Jianxin Fu ◽  
Kirk Bergstrom ◽  
Xindi Shan ◽  
J. Michael McDaniel ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Critical Role ◽  
Gastric Epithelium ◽  
Tn Antigen ◽  
Gastric Mucus ◽  
Truncated Form ◽  
Gastric Cancer Patients ◽  
Gastric Cancer Progression

Core 1–derived mucin-type O-glycans (O-glycans) are a major component of gastric mucus with an unclear role. To address this, we generated mice lacking gastric epithelial O-glycans (GEC C1galt1−/−). GEC C1galt1−/− mice exhibited spontaneous gastritis that progressed to adenocarcinoma with ∼80% penetrance by 1 yr. GEC C1galt1−/− gastric epithelium exhibited defective expression of a major mucus forming O-glycoprotein Muc5AC relative to WT controls, which was associated with impaired gastric acid homeostasis. Inflammation and tumorigenesis in GEC C1galt1−/− stomach were concurrent with activation of caspases 1 and 11 (Casp1/11)–dependent inflammasome. GEC C1galt1−/− mice genetically lacking Casp1/11 had reduced gastritis and gastric cancer progression. Notably, expression of Tn antigen, a truncated form of O-glycan, and CASP1 activation was associated with tumor progression in gastric cancer patients. These results reveal a critical role of O-glycosylation in gastric homeostasis and the protection of the gastric mucosa from Casp1-mediated gastric inflammation and cancer.

EDD1 predicts prognosis and regulates gastric cancer growth in vitro and in vivo via miR-22

2016 ◽  
Vol 0 (0) ◽  
Author(s):  
Min Yang ◽  
Nan Jiang ◽  
Qi-wei Cao ◽  
Qing Sun
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Patient Survival ◽  
Underlying Mechanism ◽  
Gastric Cancer Cells ◽  
Cancer Tissues

Abstract Gastric cancer is the most common digestive malignant tumor worldwild. EDD1 was reported to be frequently amplified in several tumors and played an important role in the tumorigenesis process. However, the biological role and potential mechanism of EDD1 in gastric cancer remains poorly understood. In this study, we are aim to investigate the effect of EDD1 on gastric cancer progression and to explore the underlying mechanism. The results showed the significant up-regulation of EDD1 in -gastric cancer cell tissues and lines. The expression level of EDD1 was also positively associated with advanced clinical stages and predicted poor overall patient survival and poor disease-free patient survival. Besides, EDD1 knockdown markedly inhibited cell viability, colony formation, and suppressed tumor growth. Opposite results were obtained in gastric cancer cells with EDD1 overexpression. EDD1 knockdown was also found to induce gastric cancer cells apoptosis. Further investigation indicated that the oncogenic role of EDD1 in regulating gastric cancer cells growth and apoptosis was related to its PABC domain and directly through targeting miR-22, which was significantly down-regulated in gastric cancer tissues. Totally, our study suggests that EDD1 plays an oncogenic role in gastric cancer and may be a potential therapeutic target for gastric cancer.

scholarly journals The Diagnosis Value of Promoter Methylation of UCHL1 in the Serum for Progression of Gastric Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Gongping Wang ◽  
Wei Zhang ◽  
Bo Zhou ◽  
Canhui Jin ◽  
Zengfang Wang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Promoter Methylation ◽  
Poor Prognosis ◽  
Methylation Status ◽  
Tumor Stage ◽  
Chronic Atrophic Gastritis ◽  
Dependent Manner ◽  
Specific Pcr ◽  
And Control

Background.Aberrant promoter methylation has been considered as a potential molecular marker for gastric cancer (GC). However, the role of methylation of FLNC, THBS1, and UCHL1 in the development and progression of GC has not been explored.Methods.The promoter methylation status of UCHL1, FLNC, THBS1, and DLEC1 was assessed by quantitative methylation-specific PCR (QMSP) in the serum of 82 GC patients, 46 chronic atrophic gastritis (CAG) subjects, and 40 healthy controls.Results.All four genes had significantly higher methylation levels in GC patients than in CAG and control subjects. However, only UCHL1 methylation was significantly correlated with the tumor stage and lymph node metastasis. While THBS1 methylation was altered in an age-dependent manner, FLNC methylation was correlated with differentiation andHelicobacter pyloriinfection. DLEC1 methylation was only associated with tumor size. Moreover, methylated UCHL1 with or without THBS1 in the serum was found to be significantly associated with a poor prognosis.Conclusion.The promoter methylation degree of FLNC, THBS1, UCHL1, and DLEC1 in serum could tell the existence of GC and only UCHL1 in the serum was also associated with poor prognosis of GC.

scholarly journals LncRNA ELFN1-AS1 Upregulates TRIM29 to Promote Gastric Cancer Progression by Suppressing miR-211-3p

2021 ◽  
Author(s):  
Jinxi Huang ◽  
Weiwei Yuan ◽  
Beibei Chen ◽  
Gaofeng Li ◽  
Xiaobing Chen
Keyword(s):  
Gastric Cancer ◽  
Cancer Progression ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Vitality ◽  
Reverse Transcription Quantitative Pcr ◽  
Fibronectin Type Iii ◽  
Fibronectin Type Iii Domain ◽  
Cancer Tissues

Abstract BackgroundExtracellular leucine rich repeat and fibronectin type III domain containing 1-antisense RNA 1 (ELFN1-AS1) was upregulated in tumors. Nevertheless, the biological functions of ELFN1-AS1 in gastric cancer are not fully understood.MethodsThe ELFN1-AS1, miR-211-3p and TRIM29 expression levels were determined by reverse transcription-quantitative PCR. CCK8, EDU and colony formation assays were done to test the GC cell vitality. The migratory and invasive capabilities of GC cells were further measured by transwell invasion and cell scratch assays. The ceRNA activity of ELFN1-AS1 for TRIM29 via miR-211-3pp was ascertained through pull down, RIP and luciferase reporter assays.ResultsELFN1-AS1 and TRIM29 were robustly expressed in gastric cancer tissues and negatively associated overall survival time of patients. The ELFN1-AS1 silence blocked the proliferation, migration and invasion of GC cells. The oncogenic role of ELFN1-AS1 was recognized to be modulated by miR-211-3pp, which competitively bind to 3'UTR TRIM29 and resulted in the reduced expression of TRIM29.ConclusionELFN1-AS1 maintained the tumorigensis of GC cells by ELFN1-AS1/miR-211-3pp/TRIM29 axis, suggesting that intervention targeting this axis may be warranted for GC treatment.

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