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.
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.
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).
From these results, it was suggested that PPARgamma activation might suppress COX-2 expression via the nuclear factor-kappaB pathway in the ovarian carcinoma cells and that low expression of PPARgamma and high expression of COX-2 might be involved in carcinogenesis and progression of ovarian tumours.
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.
The purpose of the study was to determine the capability of the midkine (MK) and cycooxygenase-2 (cox-2) gene promoter regions to function as tumor-specific promoters for use in targeted gene therapy of ovarian cancer.