Upregulation of SIRT1 gene in gastric adenocarcinoma

Özcan, Önder; Belli, Aslı Akın; Çetin, Esin Sakallı; Kara, Murat; Çelik, Özgür; Kaplan, Mehmet; Kayilioglu, Selami Ilgaz; Dönmez, Cem; Polat, Murat

doi:10.5152/tjg.2019.18550

Cited by 8 publications

(12 citation statements)

References 23 publications

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“…For example, some studies have found that SIRT1 expression was downregulated in GC patients with a poor prognosis (1,19). However, other studies have reported that SIRT1 levels in GC tissue were high, which is associated with epithelial-mesenchymal transition (EMT), cell invasion, as well as poor prognosis (5,12). Our previous paper supported the latter finding.…”

Section: Original Articlesupporting

confidence: 81%

“…SIRT1, a class III histone deacetylase (5,15,16), has been reported to be associated with the pathogenesis of neoplastic, metabolic, infectious, and neurodegenerative diseases (15,17). Recently, there has been some debate concerning the role of SIRT1 in the progression of GC (18).…”

Section: Original Articlementioning

confidence: 99%

“…The incidence of gastric cancer (GC) is declining worldwide (1)(2)(3). However, survival length and quality of life remain poor in some patients (1,4,5). Further, little is known about the pathogenesis and mechanism underlying the metastasis process.…”

Section: Introductionmentioning

confidence: 99%

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Candidate oncogene circularNOP10 mediates gastric cancer progression by regulating miR-204/SIRT1 pathway

Xu¹,

Wang²,

Wang³

et al. 2021

J Gastrointest Oncol

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Background: The role of circular RNA (circRNA) in gastric cancer (GC) is attracting increasing attention. CircNOP10 (hsa_circ-0034351) has been reported to be upregulated in human GC tissue. However, the biological role and mechanism of circNOP10 in GC remain unknown. Methods: Circular RNA expression profile of GC was detected based on microarray, and circNOP10 was identified for the subsequent investigation. Clinical samples of GC tissue and patient blood were obtained from the Zhongda Hospital, Southeast University. The different degraded GC cell lines were presented in our laboratory. The function and mechanism of circNOP10 in GC were investigated using Western blot, qRT-PCR, flow cytometry, in situ hybridization and pull down experiment. Results:The results indicated that increased circNOP10 in GC tissue was involved in tumor stage and prognosis. In addition, circNOP10 sponged microRNA-24 (miR-204)-mediated biological processes through sirtuin 1 (SIRT1), which further confirmed that the circNOP10/miR-204/SIRT1 pathway promoted proliferation and migration as well as epithelial-mesenchymal transition (EMT) through the NF-κβ pathway in GC cell lines. Conclusions: Candidate oncogene circNOP10 mediated GC cell proliferation, arrest cell cycle in G 2 /M phase, induced cell apoptosis, enhanced tumor metastasis, as well as EMT by activating the miR-204/SIRT1 pathway, suggesting that it may serve as a potential biomarker in GC therapy.

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Section: Original Articlesupporting

confidence: 81%

Section: Original Articlementioning

confidence: 99%

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Candidate oncogene circularNOP10 mediates gastric cancer progression by regulating miR-204/SIRT1 pathway

Xu¹,

Wang²,

Wang³

et al. 2021

J Gastrointest Oncol

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“…Gastric cancer (GC) is an aggressive malignancy with an extremely poor prognosis and a high incidence [ 1 ]. The incidence of gastric adenocarcinoma (GAC) accounts for 95 percent of gastric malignant tumors [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

SPP1 Regulates Radiotherapy Sensitivity of Gastric Adenocarcinoma via the Wnt/Beta-Catenin Pathway

Sun

Shang

Liu

2021

Journal of Oncology

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Purpose. Radiotherapy has been widely applied for the treatment of locally advanced and metastatic gastric adenocarcinoma (GAC). The aberrant expression of secreted phosphoprotein 1 (SPP1) is involved in radiosensitivity in a variety of cancers. The present study aims to characterize the clinical significance of SPP1 expression in GAC and its role and underlying mechanism of radiosensitivity. Methods. The SPP1 expression in GAC tissues and pericarcinomatous tissues was determined by QRT-PCR and immunohistochemistry, and the SPP1 expression in GAC cell lines (BGC823, AGS, and SGC7901) and normal human gastric epithelial cell line (GES-1) was determined by western blot. T-test, one-way ANOVA, Cox regression model, and Kaplan–Meier plotter were applied to further assess the association between SPP1 expression and the prognosis of the patients with GAC. After irradiation and transfection with si-SPP1 combined with or without Wnt/β-catenin pathway inhibitor (XAV939), western blot, transwell, flow cytometry, and TOP-flash reporter assay were applied to detect DNA damage, invasion, apoptosis, cell cycle, and activation of Wnt/β-catenin pathway, respectively. Results. SPP1 mRNA and protein levels in GAC tissues were both dramatically higher than those in pericarcinomatous tissues. SPP1 overexpression was positively associated with tumor size, nodal status, and histological grade of GAC patients. SPP1 overexpression, depth of invasion, and nodal status were independent prognostic factors for the patients. High SPP1 expression was negatively related to the overall survival in patients with GAC. We found that SPP1 knockdown enhanced the radiosensitivity of GAC cell lines (AGS and SGC7901). Increasing H2AX phosphorylation, apoptosis and G2/M phase arrest, and decreasing invasion were observed after the administration of si-SPP1 and irradiation. Radiosensitivity of SPP1 was mainly dependent on the Wnt/β-catenin signal pathway. XAV939 could enhance these phenomena induced by irradiation combined with SPP1 knockdown. Conclusion. This study demonstrates that SPP1 suppresses Wnt/β-catenin signaling to enhance the radiosensitivity of GAC via inhibiting invasion and accelerating DNA damage, G2/M phase arrest, and apoptosis.

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“…In single‐center studies, GCC with SIRT1 gene overexpression was more frequently found to have lymphovascular invasion, lymph node and distant organ metastases, and poorer prognosis, compared with those without SIRT1 gene overexpression 97 . SIRT1 gene overexpression was also present in advanced GCC in Turkish patients, but not present in early GCC, poorly cohesive carcinoma or signet‐ring cell carcinoma, female patients and patients younger than 45 years old 98 . The underlying detailed molecular mechanisms on the role of the SIRT1 gene mutation in GCC tumorigenesis are unknown.…”

Section: Epidemiological Featuresmentioning

confidence: 95%

Unraveling the identity of gastric cardiac cancer

Huang

Read

Gold

et al. 2020

J of Digest Diseases

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The classification of gastric cardiac carcinoma (GCC) is controversial. It is currently grouped with esophageal adenocarcinoma (EAC) as an adenocarcinoma of the gastroesophageal junction (GEJ). Recently, diagnostic criteria for adenocarcinoma in the GEJ were established and GCC was separated from EAC. We viewed published evidence to clarify the GCC entity for better patient management. GCC arises in the cardiac mucosa located from 3 cm below and 2 cm above the GEJ line. Compared with EAC, GCC is more like gastric cancer and affects a higher proportion of female patients, younger patients, those with a lower propensity for reflux disease, a wider histopathologic spectrum, and more complex genomic profiles. Although GCC pathogenesis mechanisms remain unknown, the two-etiology proposal is appealing: in high-risk regions, the Correa pathway with Helicobacter pylori infection, chronic inflammation, low acid and intestinal metaplasia, dysplasia and carcinoma may apply, while in low-risk regions the sequence from reflux toxin-induced mucosal injury and high acid, to intestinal metaplasia, dysplasia and carcinoma may occur. In early GCC a minimal risk of nodal metastasis argues for a role of endoscopic therapy, whereas in advanced GCC, gastric cancer staging rules and treatment strategy appear to be more appropriate than the esophageal cancer staging scheme and therapy for better prognosis stratification and treatment. In this brief review we share recent insights into the epidemiology, histopathology and genetics of GCC and hope that this will stimulate further investigations in order to improve the clinical management of patients with GCC.

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Upregulation of SIRT1 gene in gastric adenocarcinoma

Cited by 8 publications

References 23 publications

Candidate oncogene circularNOP10 mediates gastric cancer progression by regulating miR-204/SIRT1 pathway

Candidate oncogene circularNOP10 mediates gastric cancer progression by regulating miR-204/SIRT1 pathway

SPP1 Regulates Radiotherapy Sensitivity of Gastric Adenocarcinoma via the Wnt/Beta-Catenin Pathway

Unraveling the identity of gastric cardiac cancer

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