We assessed the effect of celecoxib on extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase activity by a transcription factor activation assay then evaluated, if these factors might be involved in the COX-2-independent tumor-killing effect of celecoxib by blocking their activity.
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.
In summary, COX-2 -765G>C polymorphism confers ESCC susceptibility particularly in females and patients with middle third anatomical location of the tumor.
Overall, it was concluded that NSAIDs, particularly cyclooxygenase-2 (COX-2) inhibitors, might have a protective effect on CRC development and slow down progression of tumor in a DMH-induced experimental cancer model.
Furthermore, overexpression of COX-2 protein was observed in association with homozygosity in several polymorphic sites within COX-2 gene (promoter region sites -1186 T/T and -765 G/G, intron 5 IVS5-275 T/T, and exon 10 Ex10+837 T>C), indicating their role in development of these tumors.
Therefore, it was hypothesized that tumor EGFR mutation status may influence the effectiveness of simultaneous EGFR and COX-2 inhibition in patients with NSCLC.
We examined the association between statin use and colorectal cancer risk according to tumor location, KRAS mutation status, microsatellite instability (MSI) status, PTGS2 (COX-2) expression, or CpG island methylator phenotype (CIMP) status in two large prospective cohort studies, the Nurses' Health Study and Health Professionals Follow-up Study.
Cyclooxygenase-2 (COX-2) is involved in carcinogenesis, immune response suppression, apoptosis inhibition, angiogenesis, and tumour cell invasion and metastasis.
The co-expression of PTGS2 gene and M2 markers in human thyroid carcinoma highlights the possibility to counteract tumor growth through COX-2 inhibition.
To investigate the effects of COX-2 inhibition on the tumor endothelium in vitro, we isolated tumor endothelial cells (TECs) from human melanoma and oral carcinoma xenografts in mice, in which we confirmed that tumor growth was suppressed by inhibiting angiogenesis with the COX-2is NS398.
Although cyclooxygenase-2 (COX-2) has been suggested to play an important role in carcinogenesis, the effects of tumor suppressors on COX-2 gene expression and the combined antitumor effects of tumor suppressors and COX-2 inhibitors have rarely been investigated.
Since prior studies demonstrated cyclooxygenase 2 (COX-2) is necessary for DMBA/TPA tumor induction, we hypothesized that COX-2 inhibition might prevent BRAFi-accelerated skin tumors.
In the present study, we show that tumour promoter PMA-mediated induction of genes that are significantly associated with inflammation, tumour growth and metastasis, such as COX-2 (cyclo-oxygenase 2) and VEGF (vascular endothelial growth factor), is inhibited by PPARalpha ligands in the human colorectal carcinoma cell line SW620.
Moreover, COX-2 silencing was achieved ex vivo by infecting colon tissue samples with InvColi strains, leading to anti-inflammatory and anti-tumour effects.
Consistent with these changes, loss of COX-2 resulted in the abolition or the significant delay of tumor onset when the cells were injected in the mammary fat pad of severe combined immunodeficient mice.
PGE(2), synthesized by cyclooxygenase-2 (COX-2)-overexpressing tumor, is known to contribute to cellular immune suppression in cancer patients, but the mechanism remains unclear.
Growing evidence shows that Interleukin (IL)-1beta and Cyclooxygenase 2 (COX-2) play a crucial role in the pathogenesis of inflammatory diseases and tumor growth, particularly in the gastrointestinal tract.