The systemic review and cohort validation suggest that P21, COX-2, and E-cadherin are potential prognostic factors for ESCC, paving the way for more targeted prospective validation in the future.
To explore the tumor-stromal relationship in esophageal neoplasia, we examined methylation of COX-2 (PTGS2), a gene etiologically associated with the development of gastrointestinal cancers, in adjacent foci of epithelium, subepithelial lymphocytes and non-lymphocytic stromal cells found in sections of normal squamous epithelium, squamous dysplasia and invasive esophageal squamous cell carcinoma.
Collectively, the promoting action of chloroform-extract from cigarette smoke on esophageal squamous-cell carcinoma cell proliferation is beta-adrenoceptor- and COX-2-dependent.
Taken together, our findings revealed a new post-transcriptional mechanism by which CSE regulated COX-2 expression to favor cancer cell proliferation, suggesting miR-101-3p as a potential biomarker and therapeutic target for smoke-related ESCC.
The aim of the present study was to evaluate the association between cyclooxygenase-2 (COX-2), X-ray repair cross complementing group 1 (XRCC1), ras association domain family 1 (RASSF1) protein expression, clinicopathological characteristics, radiosensitivity and survival rate in 76 patients with esophageal squamous cell carcinoma (ESCC) who were treated with RT.
We examined the effects of celecoxib, a COX-2 inhibitor, in enhancing the antitumor effects of chemotherapy and radiotherapy for esophageal squamous cell carcinoma (ESCC) by reducing the COX-2 activity.
This study provides evidence that COX-2 is upregulated in the majority of cases of squamous dysplasia and SCC of esophagus, and that NS-398 can inhibit growth and induce apoptosis via activating caspase-3 activity in vitro.
An increased risk of ESCC was also associated with the COX-2 -1195GA (OR=1.34, 95% CI=1.08-1.68; P=0.008), -1195AA (OR=1.72, 95% CI=1.35-2.20; P=<0.001), and -765GC (OR=2.24, 95% CI=1.59-3.16; P<0.001) genotypes.
We examined the methylation status of the COX-2 promoter in five human ESCC cell lines (EC109, EC9706, KYSE 410, KYSE 150, TE-1) using bisulfite sequencing analysis.
Cyclooxygenase-2 (COX-2) is overexpressed in various types of human malignancies including squamous cell carcinomas (SCCs) of the esophagus, but little is known about COX-2 expression in premalignant esophageal squamous dysplasia.
The aim of the current study was to elucidate a further finding on the clinicopathologic significance of immunohistochemical expression of cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF), and epidermal growth factor receptor (EGFR) in Chinese patients with ESCC.
TE13 human esophageal squamous cell carcinoma cells were transfected with a COX-2 constitutive expression vector, and stable transfectants overexpressing COX-2 were established.
Real-time PCR and Western blotting were performed to detect mRNA and protein expression of APE-1 and p-signal transducer and activator of transcription 3 (STAT3) expression in MCP-1-stimulated ESCC cell lines (KYSE 220 and EC-GI-10). siRNA for APE-1 was treated to determine the role of APE-1 in the regulation of COX-2 expression, VEGF production, and antiapoptotic effect against cisplatin.
Our results suggest that COX-2 expression correlates with VEGF expression and might be a useful prognostic factor for more frequent tumor recurrence in ESCC patients undergoing neoadjuvant CRT.