Our findings showed that RARβ2 was frequently methylated in colorectal cancer and correlated with a worse prognosis and high expression of COX-2 suggesting a link between these two proteins in colorectal carcinogenesis.
COX-2 plays a very critical role in ESCC carcinogenesis, and COX-2 siRNA combined with aspirin has the potential to be an anticancer therapy for the treatment of ESCC.
These results indicated that transcriptional changes of GSTP1, PSCA and PTGS2 induced by DEHP exposure might be contribute to the increasing susceptibility of prostate carcinogenesis in late life.
Thus, the supply of arachidonic acid provided by PLA2-II/cPLA2 seems not to be the rate limiting step in PGE2 (a prostaglandin/mitogen) formation via COX-2 and PLA2-II plays a minor or no role in human colorectal carcinogenesis.
Overall, results to date support the hypothesis that long-chain omega-3 PUFAs may impact prostate inflammation and carcinogenesis via the COX-2 enzymatic pathway.
COX-2 expression in tumour cells has been associated with carcinogenesis in many human neoplasms, including head and neck cancer, while the COX-1 isoform of the cyclooxygenase enzyme is constitutively expressed in normal tissues.
Cyclooxygenase-2 (COX-2) is involved in carcinogenesis, immune response suppression, apoptosis inhibition, angiogenesis, and tumor cell invasion and metastasis.
Studies with the Min and APC-knockout mice provide the strongest evidence to date that the enzyme cyclooxygenase-2 plays a major role in colon carcinogenesis, and that nonsteroidal anti-inflammatory drugs that target cyclooxygenase-2 have great potential as colon cancer chemopreventive agents.
However, loss of function at either level of COX-2 gene regulation promotes constitutive COX-2 overexpression which plays a key role in carcinogenesis, particularly colorectal tumorigenesis.
Cyclooxygenase-2 (COX-2) involves in multiple processes in carcinogenesis, including inflammation, apoptosis inhibition, immune response suppression, tumor cell invasion, and angiogenesis.
Overexpression of COX-2 is proved to contribute to tumor promotion and carcinogenesis through stimulating cell proliferation, inhibiting apoptosis and enhancing the invasiveness of cancer cells.
Cyclooxygenase-2 (COX-2), as a potential target of cancer chemoprevention, has been played pivotal roles in proliferation of tumor cells and carcinogenesis.
Cyclooxygenase-2 (COX-2) is proven to influence the carcinogenesis through immune response suppression, apoptosis inhibition, angiogenesis regulation, and tumor cell invasion.
How COX-2 overexpression results in tumorigenesis and how COX-2 selective agents mediate their chemopreventive effects are issues that remain poorly understood.
There is considerable interest in the involvement of cyclooxygenase-2 (COX-2) in colon carcinogenesis and its progression, because nonsteroidal anti-inflammatory drugs (NSAIDs) reduce mortality from colon cancer and COX-2 is one of the known targets of NSAIDs.
The aim of this study is to investigate (1) whether expression of COX-2 and PPARgamma is associated with ovarian carcinogenesis and progression of ovarian tumours and (2) whether COX-2 expression is controlled through ligand-mediated activation of PPARgamma in ovarian carcinoma cells.
We aimed to determine the expression and functional activity of TLR4 in the esophagus and whether TLR4 activation in BE could promote carcinogenesis by inducing COX-2 expression.