Anticancer Effect and Apoptosis of All-trans-retinoic Acid on the Human Ovarian Epithelial Carcinoma Cell Lines.
- Author:
Jee Young HAN
;
Woo Hee JUNG
;
Tai Seung KIM
- Publication Type:Original Article
- Keywords:
Ovarian carcinoma;
tRA;
Anticancer effect;
Apoptosis
- MeSH:
Apoptosis*;
Blotting, Northern;
Cell Line*;
DNA;
Electrophoresis;
Female;
Gene Expression;
Genes, bcl-2;
Genes, myc;
Genes, p53;
Humans*;
Receptors, Retinoic Acid;
Tretinoin*
- From:Korean Journal of Pathology
2000;34(3):225-234
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Ovarian carcinoma is a serious disease in women. Some reports revealed all-trans-retinoic acid (tRA) inhibited the proliferation of ovarian carcinoma cell lines and induced apoptosis. The aim of this study was to evaluate the anticancer and apoptotic effects of tRA and the expression of the retinoic acid receptor (RAR) alpha, beta, gamma, p53, bcl-2, and c-myc genes on the ovarian carcinoma cell lines, NIH OVCAR3 and SKOV3. In both cell lines, the proliferation of tumor cells was inhibited and characteristic morphologic patterns of apoptosis were shown after treatment of tRA. The number of apoptotic cells and the percentage of apoptosis were increased after treatment of tRA. The gel electrophoresis revealed the DNA ladder pattern in the NIH OVCAR3. Gene expressions were observed using northern blotting. There was no RARalpha expression in both cell lines. In NIH OVCAR3, there was no changes in the expression of RARbeta and bcl-2 gene. The RARgamma gene expression of tRA treated group was slightly increased, but p53 gene expression was decreased, and c-myc gene was not expressed. In SKOV3, the expressions of RARbeta, gamma, and p53 genes were increased and that of bcl-2 was decreased in the tRA treated group. There was no change in c-myc gene expression. These results suggest tRA has anticancer and apoptotic effect on both ovarian carcinoma cell lines. RARbeta, RARgamma, bcl-2, and p53 gene expressions were correlated with these effects of tRA on SKOV3 but not on NIH OVCAR3.