In the present study, we tested hypothesis that COX-2 induces loss of expression of E-cadherin, with resulting promotion of cancer cells' invasiveness in ovarian cancer.
These results showed the patients with higher COX-2 expression had a significantly poorer survival rate, COX-2 expression had the potential to be a prognostic marker of ovarian cancer.
The aim of the present study was to investigate the effects of plasmid-mediated RNA interference targeting of cyclooxygenase-2 (COX-2) on the biological behaviors of SKOV3 human ovarian cancer cells and to analyze the function of COX-2 in carcinogenesis and development of ovarian cancer.
In conclusion, the present study demonstrated that RNAi can effectively silence COX‑2 gene expression and inhibit the growth of ovarian cancer cells, which indicates that there is a potential of targeting COX‑2 as a novel gene therapy approach for the treatment of ovarian cancer.
The association of PTGS2rs5275 with nonserous ovarian carcinoma and possible effect modification by NSAID use needs further validation, preferably in prospective studies.
For 15-lipoxygenase-1 and cyclooxygenase-2, we did not observe differential expression, but there was a trend for increased steady-state concentrations of cyclooxygenase-1 (P=0.1 for ovarian carcinoma, P=0.011 for metastases) and 5-lipoxygenase (P=0.1 for ovarian carcinoma, P=0.018 for metastases, respectively).
LPA contributes to the development, progression, and metastasis of ovarian cancer in part by inducing the expression of genes that contribute to proliferation, survival, or invasion, including cyclooxgenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2).
Cyclooxygenase-1 and cyclooxygenase-2 are enzymes involved in the production of prostaglandins and play a role in the regulation of tumor progression in several malignancies, including ovarian carcinomas.
Overexpression of the embryonic-lethal abnormal vision-like protein HuR in ovarian carcinoma is a prognostic factor and is associated with increased cyclooxygenase 2 expression.
Pharmacological blockade of the ET(A)R is an attractive strategy to control COX-2 induction, which has been associated with ovarian carcinoma progression and chemoresistance.
These results suggest that COX-2 expression might play an important role in ovarian cancer development and that COX-2 expression in ovarian adenocarcinomas is frequently associated with p53 protein accumulation.
Whether COX-2 inhibitor therapy would be beneficial in the prevention and/or treatment of ovarian cancer, the most lethal gynecological malignancy worldwide, is not known.