The megameric conjugate with nimesulide was tested in vitro on three human cell lines: squamous cell carcinoma (SCC-15) and glioblastoma (U-118 MG) overexpressing cyclooxygenase-2 (COX-2), and normal skin fibroblasts (BJ).
COX-2 was neo-expressed in 86.6% of the cases and expression progressively increased from ePP to ePSCC (P = 0.0003) and from well to poorly differentiated (P = 0.033).
Moreover, we found that p62 stabilizes COX-2 protein through the p62 ubiquitin-associated domain and that p62 regulates prostaglandin E<sub>2</sub> production <i>in vitro</i> In a syngeneic squamous cell carcinoma mouse model, p62 knockdown inhibited tumor growth and metastasis.
The present study was undertaken to evaluate two such components of the inflammatory milieu, tumor-associated tissue eosinophilia (TATE) as well as Cyclo-oxygenase-2 (COX-2) gene expression, quantitatively in oral squamous cell carcinoma (OSCC) patients in relation to treatment outcomes and patterns of recurrence.
Subgroup analysis also indicated that Cox-2 expression was significantly correlated with skin cancer with the pathology type of squamous cell carcinoma (OR = 31.95, 95% CI: 15.08-67.72, P < 0.05) and basal cell carcinoma (OR = 14.69, 95% CI: 4.80-44.94, P < 0.05).
Factors predicting outcome after salvage treatment for stage IV oral squamous cell carcinoma: Evidence of the potential importance of the cyclooxygenase-2-prostaglandin E2 pathway.
The goal of our study was a comparative evaluation of apoptosis regulators: p53, Bcl-2, Bax, COX-2, and survivin in lung adenocarcinoma (AC) and squamous cell carcinoma (SCC).
In a combination regimen, Sabutoclax and COX-2 inhibitor, Celecoxib, synergistically inhibited the growth of OSCC in vitro and also significantly reduced OSCC tumor growth in vivo.
There was a strong association between COX-2 overexpression and recurrence of oral squamous cell carcinoma (P < 0.001) and a positive relation between increased MDM2 expression and failure of radiotherapy (P = 0.007).
In contrast, GPR109A activation in keratinocytes induces flushing by activation of Cox-2-dependent inflammatory signaling, and the receptor expression is upregulated in human epidermoid carcinoma.
Results of the present study indicate that these three functional variants in the COX-2 regulatory region may contribute to risk modification of tobacco-related oral squamous cell carcinoma in Asian Indians.
We investigated possible relations between COX-2 and NO with the use of a human epidermoid carcinoma cell line, designated KB, in which overexpression of COX-2 protein was induced by gene transfer.