COX-2

Simple information:
PTGS2 (reccomended name) or COX-2 (common name) is a gene that codes for the
enzyme Prostaglandin-endoperoxide synthase 2 also called cyclooxygenase-2. It is
mainly associated with responses to physiological stresses such as infection and
inflammation (R,R2).
A several number of studies indicates that PGTS2 is associated with an increasing in
colorectal (R,R2,R3), prostate (R) and breast cancer risk (R). In particular many
evidences suggest that PTGS2 is probably involved in tumor proliferation and
growth, in the formation of metastases and in the resistance of cancer cells to
programmed death (R1,R2,R3).
Recent studies suggest that PTGS2 is linked with the development of type 2 diabetes
mellitus (R) and with the promotion of retinal phatologes in diabetes (R).
Advanced information:
PTGS2 (COX-2), converts arachidonic acid (AA) to prostaglandin endoperoxide H2.
Prostaglandines are mediator in the sinthesis of prostanoids which are responsable
for cell adhesion to extracellular matrix proteins, inflammation and fine-tuning of
physiological processes requiring instantaneous, continuous regulation (R, R2).
PGHS2 are targets for NSAIDs (non-steroidal anti-inflammatory drugs) and specific
inhibitors called coxibs (R1,R2).
Potential simple fixes:
Use of NSAIDs such as Iburprofen, Aspirin and Bromfenac. It is
demonstrated that chronic inflammation predisposes to biliary tract (and
other type of) cancer and that use of non-steroidal anti-inflammatory drugs is
protective (R).
Use of COX-2 specific inhibitors such as Celecoxib and Lumiracoxib.
Although the pharmaco-based prescription of this inhibitors needs further
investigations (R), their anti-proliferative action is confirmed in tumor cells
with an abnormal concentration of PGTS2 (R).
Glucosamine hydrochloride seems to specifically inhibits COX-2 (R).

Potential Advanced Fixes:

A study suggest that diet could affect responses to inhibitor-COX drugs.
Indeed the fatty acid tone of cells could importantly influence basal
prostanoid formation and then ameliorate NSAIDs action or cause adverse
side effects. Dietary studies need to be performed (R).
Progesterone may inhibit NF-kappaB activation of COX-2 gene
expression and uterine contractility (R).
Treatment with retinoic acid or carnosol, two structurally unrelated
compounds with anticancer properties, inhibited COX-2 expression in human
mammary epithelial cells (R).