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Introduction bladder transitional cell carcinoma is the most common malignancy of the urinary system . Therefore , in-depth study of the pathogenesis of bladder cancer , explore effective preventive measures and new ways to have important anti-cancer therapy . The occurrence of bladder cancer , the development is a multi- factor , multi-stage process of sexual development . Its occurrence may be caused by a variety of factors to the bladder mucosal epithelial hyperplasia , cancer -related . Bladder mucosal repair process prostaglandin E 2 ( the prostaglandin E 2 < / sub > , PGE 2 < / sub > ) , increase of PGE 2 clear mucosal protection and repair , and cell updates , and possibly by affecting mitosis , inhibition of apoptosis , reduce cancer immune surveillance . Oxidase (cyclooxygenase, COX) is the rate-limiting enzyme in arachidonic acid synthesis of PGE 2 of . COX divided into structured COX-1 and inducible COX - 2 . COX-2 is synthesized in the cells by inflammatory mediators , growth factors, induced by carcinogenic agents factors involved in inflammation, cancer and other pathological processes can be reduced to the extracellular matrix, and beneficial to tumor growth and metastasis . COX-2 by upregulating vascular endothelial growth factor . (Vascular endothelial growth factor , VEGF) expression and play a role in promoting angiogenesis , VEGF is the strongest angiogenic factors , while vascular permeability agents , hydrolysis matrix film to promote tumor neovascularization formed to promote tumor growth and metastasis . The aim of the present study was to investigate the expression of COX - 2 and VEGF in the occurrence of bladder cancer , the role of the invasion , the relationship between the two , and clinical pathological significance for the occurrence of bladder cancer invasion prediction and prognosis . Open up new avenues of treatment of tumors : clinical application of selective COX-2 inhibitors and anti-angiogenic targeted therapy provide a theoretical basis for the clinical .
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