The link between obesity and mammary carcinogenesis involves elevated estrogen production and proinflammatory stimuli within the adipose tissue, with activation of the cyclooxygenase-2 pathway.
However, COX-2 also suppresses skin tumorigenesis and their relationship with SIRT6, making it an interesting target for the discovery of drugs with anti-inflammatory and anti-cancer properties.
In the Apc<sup>Min/+</sup> model of familial adenomatous polyposis (MMR-proficient CRC), increased Cyclooxygenase-2 (Cox-2) expression by cells which include alternatively activated mononuclear phagocytes promotes intestinal tumorigenesis by mechanisms which may include immune suppression.
Hyperproduced prostaglandin E<sub>2</sub> by cyclooxygenase-2 and microsomal prostaglandin E synthase-1 evokes several pathophysiological responses such as inflammation and carcinogenesis.
We have shown that nanoDEN, same as diethylnitrosamine (DEN), induced overexpression of multiple pivotal factors (including COX-2, β-catenin and PCNA) during oncogenesis.
In conclusion, COX-2 and survivin expression is positively associated with the pathological grade of a glioma and may contribute to glioma tumorigenesis.
These findings indicated that COX-2 and 15-PGDH, the two enzymes that regulate PGE<sub>2</sub> levels, were significantly altered in gastric cancer, and that <i>H. pylori</i> may contribute to gastric carcinogenesis through modulating COX-2 and 15-PGDH mRNA expression and protein synthesis.
The objective of the present work is to investigate the anti-inflammatory mechanism of action of PE during DMBA rat mammary carcinogenesis by evaluating the expression of cyclooxygenase-2 (COX-2), heat shock protein 90 (HSP90), nuclear factor-κB (NF-κB) and nuclear factor erythroid 2p45 (NF-E2)-related factor 2 (Nrf2).
COX-2 expression induces carcinogenesis and is thought to be an adverse prognostic factor in gastric carcinomas while the prognostic value of DNA mismatch repair (MMR) is still controversial.
Our study adds additional evidence that the COX-2 pathway is involved in pancreatic carcinogenesis and suggests that urinary PGE-M may serve as a biomarker for predicting pancreatic cancer risk.
Considering the important role of COX2 in tumorigenesis and thrombosis, and the large number of circulating platelets, we propose that platelet COX2 may play an important role in physiologic and pathologic conditions.
In the present review, we provide published evidence to demonstrate that (1) COX-2 signaling plays a major role in the progression of colorectal cancer, (2) activation of COX-2 in the stromal compartment also contributes to colorectal carcinogenesis, and (3) inhibition of COX-2 signaling by COX-2 inhibitors might be an effective method to control colorectal cancer.
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.
Paracrine cyclooxygenase-2 activity by macrophages drives colorectal adenoma progression in the Apc <sup>Min/+</sup> mouse model of intestinal tumorigenesis.
Previous studies indicate that COX-2, one of the isoforms of COX, is highly expressed in colon cancers and plays a key role in colon cancer carcinogenesis.