Subdistribution hazard ratio (SHR) of GC with statins was calculated by competing risk regression with propensity score (PS) analysis matching 19 variables (age, sex, comorbidities and other drug usage including proton pump inhibitors, non-steroidal anti-inflammatory drugs, aspirin, cyclooxygenase-2 inhibitors, and metformin).
Finally, we demonstrated that combinatorial inhibition of COX-2 and DNMT using Celecoxib and Decitabine synergistically inhibited GC growth <i>in vitro</i> and <i>in vivo</i>.
Double IHC staining showed that TAMs were aggregated near GC tumor nests and had high COX2 expression; moreover, the number of TAMs that infiltrated the tumor nest was correlated with the depth of invasion, COX2 expression and poor prognosis in human GC.
This meta-analysis of 15 case-control studies provides strong evidence that the COX-2rs20417 polymorphism increases the risk of GC susceptibility in general populations, especially in Asians.
The COX2 -1195G > A polymorphism showed significant correlation with gastric cancer susceptibility in total analysis, and stratification analysis by ethnicity also revealed a similar association in both Asian and Caucasian groups under the same contrast.
The results revealed that CDH1, cyclooxygenase-2 and matrix metalloproteinase genes had significantly higher expression levels, whereas the expression levels of dermatopontin and transforming growth factor β receptor 2 were decreased in GC samples.
Combined administration of γ-secretase and COX-2 inhibitor produced a marked inhibition of growth in AGS cells, which suggests that patients with poorly differentiated GC may benefit from the blockage of NICD, which potentially serves a role in GC differentiation.
Our results demonstrate the unregulated expression of ANXA1 and COX-2 in precursor lesions of esophageal and stomach cancers, reinforcing their involvement in gastroesophageal carcinogenesis.
The meta-analysis results showed that the COX-2 -1195G>A gene polymorphism significantly correlated with an increased risk of gastrointestinal cancers, particularly gastric cancer (A <i>vs</i> G: OR = 1.35; AA/AG <i>vs</i> GG: OR = 1.54; AA <i>vs</i> GG/AG: OR = 1.43; AA <i>vs</i> GG: OR = 1.80; AG <i>vs</i> GG: OR = 1.35).
Cell proliferation and migration experiments were conducted on the RhoA-silenced A6-B9 cells and COX-2-silenced D7-B8 cells so as to discuss their role in the development of gastric cancer.
In 180 cases of GC, the clinicopathologic features were correlated with the results obtained after paired immunohistochemical stains (tumor/normal mucosa) with 15 antibodies: E-cadherin, HER-2, VEGF, CD31, CD105, COX-2, maspin, bax, bcl-2, p53, Ki67, MLH-1, MSH-2, Mena protein, and vimentin.
Our findings emphasize the importance of COX-2 as a potential marker of tumor progression and prognosis in GC, and that the inhibition of COX-2 activity may have a therapeutic benefit in GC.
A pathway analysis of human gastric cancer shows that both the COX-2 pathway and Wnt/β-catenin signaling are significantly activated in tubular-type gastric cancer, and basal levels of these pathways are also increased in other types of gastric cancer.
Although an association between candidate SNPs and gastric cancer was not found in Peruvians, trend in our data is consistent with meta-analyses results that suggest PTGS2-rs689466-A is associated with H. pylori-associated gastric cancer in East Asia.