An inducible enzyme, not found in normal tissues in more than minute quantities.

Cyclooxygenases are a family of myeloperoxidases located at the luminal side of the endoplasmic reticulum and nuclear membrane.

Cyclooxygenases regulate a rate-limiting step of biosynthesis of prostaglandins from arachidoninc acid.

Cyclooxygenases enzymes convert arachidonic acid to prostatglandin G2, and prostaglandin H2 and further to prostaglandin D2, F2alpha, E2, and I2 and thromboxane A2.


Prostaglandins are produced following the sequential oxygenation of arachidonic acid, docosahexaenoic or eicosapentaenoic by cyclooxygenases (COX-1 and COX-2) and terminal prostaglandin synthases.

Two forms of cyclooxgenases are identified COX-1 and COX-2.

COX-1 plays a role in tissue homeostasis by modulating cell proliferation, angiognesis, and platelet aggregation by thromboxane production.

COX-2 is the inducible isoform of cyclooxygenases and its overexpression is linked to various cancers.

Prostaglandins act to mediate physiologic functions such as vasodilation, renal homeostasis, fever, pain sensitivity and inflammation.

Main enzyme responsible for the production of prostacyclin in the vasculature, which is an antagonist of platelet aggregation and is a vasodilator.

Found in inflammation and in many epithelial cancer cells where it is upregulated and produces prostaglandins.

Overexpression is observed in approximately 2/3 adenomas and colorectal cancers, compared with healthy colon epithelium.

Overexpression observed in malignant tissues and promotes cell-cycle progression, tumor invasiveness, and angiogenesis.

Overepression associated with decreased cell-mediated immunity.

Expression is tightly regulated and inducible by inflammation.

Increased expression in many malignant tumors and is related to poor prognosis.

Over expression occurs in malignant mesothelioma and nonsteroidal anti-inflammatory drugs specific for COX-2 have antiproliferative effects.

Elevated expression seen in breast tissue supports a protective role of aspirin and other NSAIDs against breast cancer.

May have a role in the etiology of breast cancer as prostaglandins have the ability to induce the expression of aromatase, which converts androgens to estrogens in breast tissue.

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