Cyclooxygenase-2 and Gastric Cancer

Thiel, Alexandra; Mrena, Johanna; Ristimäki, Ari

doi:10.1007/s10555-011-9312-1

Cited by 55 publications

(45 citation statements)

References 89 publications

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“…This results in the enhanced synthesis of prostaglandins in neoplastic and inflamed tissues (Coussens and Werb, 2002). Overexpression of COX-2 has been demonstrated in several adult epithelial tumors such as colon cancer (Lai et al, 2004), gastric cancer (Thiel et al, 2011) and hepatocellular carcinoma (Ogunwobi and Liu, 2011). COX-2 is linked to tumor-promoting effects, including tumor growth and metastasis, by stimulating invasiveness and angiogenesis (Chen et al, 2009;Liu et al, 2011), inhibiting apoptosis and immune surveillance (Ohno et al, 2005), and enhancing drug resistance (Mehar et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Effects of Celecoxib on Cycle Kinetics of Gastric Cancer Cells and Protein Expression of Cytochrome C and Caspase-9

Wang¹,

Niu²,

Li³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Objective: This investigation aimed to determine effects of celecoxib on the cell cycle kinetics of the gastric cancer cell line MGC803 and the mechanisms involved by assessing expression of cytochrome C and caspase-9 at the protein level. Methods: Cell proliferation of MGC803 was determined by MTT assay after treatment with celecoxib. Apoptosis was assessed using fluorescence staining and cell cycle kinetics by flow cytometry. Western blotting was used to detect the expression of caspase-9 protein and of cytochrome C protein in cell cytosol and mitochondria. Results: Celecoxib was able to restrain proliferation and induce apoptosis in a dose-and timedependent manner, inducing G0/G1 cell cycle arrest, release of cytochrome C into the cytosol, and cleavage of pro-caspase-9 into its active form. Conclusion: Celecoxib can induce apoptosis in MGC803 cells through a mechanism involving cell cycle arrest, mitochondrial cytochrome C release and caspase activation.

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Section: Introductionmentioning

confidence: 99%

Effects of Celecoxib on Cycle Kinetics of Gastric Cancer Cells and Protein Expression of Cytochrome C and Caspase-9

Wang¹,

Niu²,

Li³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…A previous study demonstrated that increased COX-2 expression is an independent prognostic factor for poor prognosis and is associated with reduced survival in patients with GC (19). Therefore, increasing attention had been directed to the mechanisms of celecoxib action on GC.…”

Section: Discussionmentioning

confidence: 99%

Anti-cancer effect of low dose of celecoxib may be associated with lnc-SCD-1:13 and lnc-PTMS-1:3 but not COX-2 in NCI-N87 cells

Song

Shu

et al. 2017

Oncology Letters

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Abstract. In order to investigate the mechanism of celecoxib and whether long non-coding RNAs (lncRNAs) were involved in the effects of celecoxib treatment in NCI-N87 cells, NCI-N87 cells were treated with 15, 30 and 60 µM celecoxib and an MTT assay was performed to assess cell viability. Following treatment with 15 µM celecoxib, the cell cycle and apoptosis were analyzed by flow cytometry, and the mRNA levels of lnc-SCD-1:13, lnc-PTMS-1:3, cyclooxygenase-2 (COX-2), integrin α3 (ITGA3) and DSH homolog 1 (DVL1) were detected by reverse transcription quantitative PCR (RT-qPCR) in NCI-N87 cells. MTT analysis demonstrated that celecoxib significantly inhibited cell viability in treated cells compared with untreated cells. Flow cytometry analysis revealed that, compared with untreated cells, the percentage of cells in the G 0 /G 1 phase was significantly increased, and the percentage of cells in the S and G 2 phase was decreased. In addition, the percentage of early and late apoptotic cells was increased in cells treated with 15 µM celecoxib compared with the control. RT-qPCR analysis also demonstrated that the mRNA levels of lnc-SCD-1:13, lnc-PTMS-1:3, ITGA3 and DVL1 were increased following treatment with celecoxib (15 µM; P<0.05). However, there were no significant differences in the expression of COX-2 mRNA between cells treated with celecoxib (15 µM) and untreated cells. The present study demonstrated that a low dose of celecoxib may be involved in regulating cell growth independent of COX-2 in NCI-N87 cells. Furthermore, ITGA3 and/or DVL1 co-expressed with lnc-SCD-1:13 and lnc-PTMS-1:3 may be associated with the effects of treatment with a low dose of celecoxib in NCI-N87 cells. IntroductionGastric cancer (GC) is a common malignancy worldwide, characterized by high invasiveness and aggressiveness (1).It is estimated that there are ~990,000 new cases of GC and that ~738,000 succumb from this type of cancer per year (2). Although a number of conventional therapeutic methods, including surgical excision and chemotherapy achieve satisfactory therapeutic effects for patients with early GC, a greater number of patients with GC at an advanced stage have poor prognosis (3). Therefore, despite increasing knowledge of the genetic and biochemical basis of GC, it is also essential to search for novel therapeutic targets and to develop more effective diagnostic and treatment methods.A series of studies have reported that nonsteroidal anti-inflammatory drugs (NSAIDs) have an anti-cancer effect in various types of cancer, including breast cancer (4), esophageal cancer (5), colorectal cancer (6), prostate cancer (7) and GC (8). In addition to aspirin, celecoxib, a cyclooxygenase-2 (COX-2) inhibitor, has been demonstrated to be involved in uncontrolled cell proliferation, apoptosis, angiogenesis and metastasis (9,10). Previous studies have suggested that celecoxib is able to induce cell apoptosis through the phosphoinositide 3 kinase/Akt signaling pathway (11) and to inhibit invasion through the adenine nucleotide translocator-...

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“…COX-2 has been shown to be involved in the processes of inflammation and carcinogenesis [56], and previous studies indicate that COX-2 expression is associated with H. pylori-induced gastritis and stomach carcinogenesis in humans [57,58]. H. pylori infection and excessive salt intake synergistically enhance COX-2 and iNOS expression in the gastric mucosa of gerbils [59].…”

Section: Cox-2 Inhibitorsmentioning

confidence: 99%

Molecular Mechanism of Gastric Carcinogenesis in Helicobacter pylori-Infected Rodent Models

et al. 2014

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Since the discovery of Helicobacter pylori (H. pylori), many efforts have been made to establish animal models for the investigation of the pathological features and molecular mechanisms of gastric carcinogenesis. Among the animal models, Mongolian gerbils and mice are particularly useful for the analysis of H. pylori-associated inflammatory reactions and gastric cancer development. Inhibitors of oxidative stress, cyclooxygenase-2 (COX-2) and nuclear factor-κB, exert preventive effects on chronic gastritis and the development of adenocarcinomas in H. pylori-infected gerbils. Genetically-modified mouse models, including transgenic and knockout mice, have also revealed the importance of p53, COX-2/prostaglandin, Wnt/β-catenin, proinflammatory cytokines, gastrin and type III mucin in the molecular mechanisms of gastric carcinogenesis. Microarray technology is available for comprehensive gene analysis in the gastric mucosa of mouse models, and epigenetics, such as DNA methylation, could be an alternative approach to correlate the observations in animal models with the etiology in humans.

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Cyclooxygenase-2 and Gastric Cancer

Cited by 55 publications

References 89 publications

Effects of Celecoxib on Cycle Kinetics of Gastric Cancer Cells and Protein Expression of Cytochrome C and Caspase-9

Effects of Celecoxib on Cycle Kinetics of Gastric Cancer Cells and Protein Expression of Cytochrome C and Caspase-9

Anti-cancer effect of low dose of celecoxib may be associated with lnc-SCD-1:13 and lnc-PTMS-1:3 but not COX-2 in NCI-N87 cells

Molecular Mechanism of Gastric Carcinogenesis in Helicobacter pylori-Infected Rodent Models

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