On the other hand, NPX and other NSAIDs are extensively studied in terms of colorectal cancer (CRC) prevention and inhibition, since it has been evidenced that COX-2 corresponds with the risk of the tumor occurrence and growth.
Parixibox, a cyclooxygenase‑2 (COX‑2) blocker, successively reduces the expression of vascular endothelial growth factor (VEGF) in the tumor microenvironment.
In a further study, we showed that inhibition of YAP and COX-2 acted synergistically and more efficiently reduced the growth of HCC cells and tumor formation than either of them alone, suggesting that dual governing of YAP and COX-2 may lead to the discovery of promising therapeutic strategies for HCC patients via blocking this positive feedback loop.
Therefore, the aim of this study is to investigate whether COX-2 expression is associated with ameloblastoma microvascular density (MVD) and with tumor aggressiveness.
Mechanistically, metformin represses inflammatory infiltration by downregulating both COX2 and PGE2 in tumor cells.<b>Conclusions:</b> Metformin is capable of repressing prostate cancer progression by inhibiting infiltration of tumor-associated macrophages, especially those induced by ADT, by inhibiting the COX2/PGE2 axis, suggesting that a combination of ADT with metformin could be a more efficient therapeutic strategy for prostate cancer treatment.<i></i>.
Patients with a high expression of COX-2 in baseline tumor biopsies had less response to treatment of pathology compared to patients with lower expression of COX-2 in baseline tumor biopsies.
COX-2 and survivin were overexpressed in glioma tissues, and higher expression levels were observed in glioma tissues of histological grades III-IV compared with those in grade I-II tumor tissues (P<0.05); however, the expression levels were not associated with gender, age, tumor size or location (P>0.05).
Insulin-like growth factor binding protein 4 (IGFBP-4) and cyclooxygenase2 (COX-2) are associated with tumor inflammatory microenvironment which is involved in the progression of tumor.
Using a transgenic C57Bl/6 mouse model of Cox-2 over-expression driven by the chicken lysozyme locus (cLys-Cox-2), which directs integration site-independent, copy number-dependent transgene expression restricted to macrophages, we demonstrated that stromal macrophage Cox-2 in colorectal (but not small intestinal) adenomas from cLys-Cox-2 x Apc <sup>Min/+</sup> mice was associated with significantly increased tumour size (P = 0.025) and multiplicity (P = 0.025), compared with control Apc <sup>Min/+</sup> mice.
The gut microbiota-driven COX2 pathway produced the lipid mediator PGE<sub>2</sub> in senescent HSCs in the tumor microenvironment, which plays a pivotal role in suppressing antitumor immunity, suggesting that PGE<sub>2</sub> and its receptor may be novel therapeutic targets for noncirrhotic NASH-associated HCC.<i>Cancer Discov; 7(5); 522-38.
Combination of anti-CTLA-4 with selumetinib negated this up-regulation of Cox-2 and Arg1, reduced the frequency of CD11<sup>+</sup> Ly6G<sup>+</sup> myeloid cells, and led to the accumulation of differentiating monocytes at the Ly6C<sup>+</sup> MHC<sup>+</sup> intermediate state in the tumor.
The COX-2 pathway promoted IBC cell migration and invasion and the CSC marker-bearing population <i>in vitro</i>, and the inhibition of this pathway reduced IBC tumor growth <i>in vivo</i>.
The antiproliferative properties of these metallic conjugates show that these compounds are potent and cancer cell selective cytotoxic agents exhibiting activity in cisplatin resistant and the COX-2 positive tumor cell lines.
Tumor-infiltrating PD-L1<sup>+</sup> cells isolated from tumor-bearing mice also exerted morphology of tumor-associated macrophages and expressed high levels of prostaglandin E<sub>2</sub> (PGE<sub>2</sub>)-forming enzymes microsomal PGE<sub>2</sub> synthase 1 (mPGES1) and COX2.
Reduced representation bisulfite sequencing (RRBS) and gene expression microarrays were performed in the HCC tumor and non-HCC liver tissues to investigate the molecular mechanisms of COX-2-driven HCC.
Previous studies by the present authors, where CRC patients were divided into high- or low-COX-2 expressing tumors, displayed important differences in the expression levels of several transcription factors involved in carcinogenesis.
Our meta-analysis demonstrates that the presence of high levels of COX-2 is associated with poor prognosis for breast cancer patients and predicts bigger tumor size and lymph node metastasis.