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Query: UMLS:C1140680 (ovarian cancer)
 28,141 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hematoporphyrin monomethyl ether (Hemoporfin) is a novel porphyrin-related photosensitizer. Photocytotoxic effect of Hemoporfin to ovarian cancer is still unclear. We used human epithelial ovarian carcinoma cell line SKOV3 and its xenograft model in nude mice to investigate the Hemoporfin-based photodynamic therapy (PDT) for ovarian cancer. The growth rates of SKOV3 cells were determined by MTT assays. Flow cytometry combined with dual Annexin V/PI staining was used to identify the death mode of the cells following PDT. We demonstrated that Hemoprofin-based PDT induced significant cell death via direct necrosis induction, and the photocytotoxity to SKOV3 cells is dose related. With SKOV3 xenograft model in nude mouse, we further demonstrated that Hemoporfin-based PDT is effective for controlling the tumor growth. Our results suggest that Hemoporfin is a promising novel photosensitizer for the treatment of ovarian cancer and merit further evaluation in the clinical practice.
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PMID:Phototoxicity of Hemoporfin to ovarian cancer. 1618 54

The studies of interaction with DNA and the cytotoxic activity of a new organometallic platinum(II) compound are presented. The ability of this new platinum complex to modify secondary DNA structure was explored by circular dichroism (CD). Electrophoretic mobility showed changes in tertiary DNA structure, and atomic force microscopy (AFM) revealed morphological changes of plasmid DNA (pBR322). This compound breaks the traditional structure-activity rules for cis-platinum compounds, but it could be of interest because of its different kinetics. An organometallic bond normally shows a trans-effect higher than that of an amine ligand, and that fact, a priori, could contribute to a higher DNA binding rate. Several ovarian cancer cell lines, resistant and non-resistant to cisplatin, were exposed to increasing concentrations of cisplatin and complex 5 for 24 h, after which time the cell number/viability was determined by the colorimetric MTT assay. A lower cytotoxicity but also a lower resistant factor was observed for organometallic compound 5 than for cisplatin, against A2780 and A2780cisR cell lines. This result is consistent with the DNA interaction degree observed by the aforementioned techniques.
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PMID:Studies of interaction of trichloro{eta2-cis-N,N-dimethyl-1-[6-(N',N'-dimethyl-ammoniummethyl)-cyclohex-3-ene-1-yl]-methylammonium}platinum(II) chloride with DNA: Effects on secondary and tertiary structures of DNA. Cytotoxic assays on human ovarian cancer cell lines, resistant and non-resistant to cisplatin. 1625 52

Curcumin, an active ingredient from the rhizome of the plant, Curcuma longa, has antioxidant, anti-inflammatory and anti-cancer activities. It has recently been demonstrated that the chemopreventive activities of curcumin might be due to its ability to inhibit cell growth and induce apoptosis. In the present study, we have investigated the effects of curcumin on growth and apoptosis in the human ovarian cancer cell line Ho-8910 by MTT assay, fluorescence microscopy, flow cytometry and Western blotting. Our data revealed that curcumin could significantly inhibit the growth and induce apoptosis in Ho-8910 cells. A decrease in expression of Bcl-2, Bcl-X(L) and pro-caspase-3 was observed after exposure to 40 microM curcumin, while the levels of p53 and Bax were increased in the curcumin-treated cells. These activities may contribute to the anticarcinogenic action of curcumin.
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PMID:Antiproliferation and apoptosis induced by curcumin in human ovarian cancer cells. 1637 85

The crude methanol extracts of Gelsemium elegans leaves were assessed for their cytotoxic activity using the microculture 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay for cellular viability. This study utilized two different types of human cancer cell lines, CaOV-3 (human ovarian cancer cells) and MDA-MB-231 (human estrogen receptor negative breast cancer cells), allowing for comparison of toxicity of G. elegans against these two cancer cells lines. Our results showed that the methanol extract of G. elegans exhibited high cytotoxicity against the human ovarian cancer cell line CaOV-3 with an IC50 value of 5microg/ml after 96 h incubation. However, G. elegans displayed discernibly less toxicity against the MDA-MB-231 cells with an IC50 value 40microg/ml after 96 h incubation and this effect was dose- and time-dependent, up to 72h and 20-30 microg/ml. In conclusion, our results demonstrated that G. elegans is potently cytotoxic against the human ovarian cancer cell line CaOV-3 and to a lesser extend towards the human breast carcinoma cancer MDA-MB-231 cells, suggesting that the extract is selective towards CaOV-3 cells and may have a chemotherapeutic role for ovarian cancer treatment in the future.
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PMID:A Study of the in vitro cytotoxic activity of Gelsemium elegans using human ovarian and breast cancer cell lines. 1649 6

Although gonadotropin-releasing hormone (GnRH) has been shown to play a role as an autocrine/ paracrine regulator of cell growth in ovarian surface epithelium and ovarian cancer, the factors which regulate the expression of GnRH and its receptor in these cells are not well characterized. In the present study, we employed real-time PCR to determine the potential regulatory effect of gonadotropins on the expression levels of GnRH I (the mammalian GnRH), GnRH II (a second form of GnRH) and their common receptor (GnRHR) in immortalized ovarian surface epithelial (IOSE-80 and IOSE-80PC) cells and ovarian cancer cell lines (A2780, BG-1, CaOV-3, OVCAR-3 and SKOV-3). The cells were treated with increasing concentrations (100 and 1000 ng/ml) of recombinant follicle-stimulating hormone (FSH) or luteinizing hormone (LH) for 24 h. Treatment with FSH or LH reduced GnRH II mRNA levels in both IOSE cell lines and in three out of five ovarian cancer cell lines (A2780, BG-1 and OVCAR-3). A significant decrease in GnRHR mRNA levels was observed in IOSE and ovarian cancer cells, except CaOV-3 cells, following treatment with FSH or LH. In contrast, treatment with either FSH or LH had no effect on GnRH I mRNA levels in these cells, suggesting that gonadotropins regulate the two forms of GnRH and its receptor differentially. In separate experiments, the effect of gonadotropins on the anti-proliferative action of GnRH I and GnRH II agonists in IOSE-80, OVCAR-3 and SKOV-3 cells was investigated. The cells were pretreated with FSH or LH (100 ng/ml) for 24 h after which they were treated with either GnRH I or GnRH II (100 ng/ml) for 2 days, and cell growth was assessed by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide] assay. Pretreatment of the cells with FSH or LH significantly reversed the growth inhibitory effect of GnRH I and GnRH II agonists in these cell types. These results provide the first demonstration of a potential interaction between gonadotropins and the GnRH system in the growth regulation of normal ovarian surface epithelium and its neoplastic counterparts.
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PMID:Differential regulation of two forms of gonadotropin-releasing hormone messenger ribonucleic acid by gonadotropins in human immortalized ovarian surface epithelium and ovarian cancer cells. 1672 89

Histone deacetylase inhibitors (HDACIs) can inhibit proliferation, induce cell cycle arrest and stimulate apoptosis of cancer cells. Our purpose was to investigate the antiproliferative effects of a novel HDACI, apicidin, on the Ishikawa endometrial cancer cell line, the SK-OV-3 ovarian cancer cell line and normal human endometrial epithelial cells. Endometrial and ovarian cancer cells were treated with various concentrations of apicidin, and the effects on cell growth, cell cycle, apoptosis and related measurements were investigated. MTT assays showed that all endometrial and ovarian cancer cell lines were sensitive to the growth inhibitory effect of apicidin, although normal endometrial epithelial cells were viable after the treatment with the same doses of apicidin that induced the growth inhibition of endometrial and ovarian cancer cells. Cell cycle analysis indicated that their exposure to apicidin decreased the proportion of cells in S-phase and increased the proportion in G0/G1 and/or G2/M phases of the cell cycle. Induction of apoptosis was confirmed by Annexin V staining of externalized phosphatidylserine and loss of the transmembrane potential of mitochondria. This induction occurred in concert with the altered expression of p21WAF1, p27KIP1, p16, cyclin A, and E-cadherin. Furthermore, apicidin treatment of these cell lines increased acetylation of H3 and H4 histone tails. These results suggest that apicidin exhibits the antiproliferative effects through selective induction of genes related to cell growth, malignant phenotype, and apoptosis. The findings raise the possibility that apicidin may prove particularly effective in the treatment of endometrial and ovarian cancers.
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PMID:Apicidin, a novel histone deacetylase inhibitor, has profound anti-growth activity in human endometrial and ovarian cancer cells. 1720 5

Using the MTT assay and the telomeric repeat amplification protocol (TRAP)-based PCR-ELISA assay, the cytotoxicity and telomerase inhibiting ability of 17 sesquiterpenes (extracted from Chinese herbs) were tested in the human ovarian cancer cell line HO-8910. The results indicated that seven sesquiterpenes inhibited cell proliferation without having an effect on telomerase activity; two sesquiterpenes inhibited neither cell proliferation nor telomerase activity; and the other eight sesquiterpenes inhibited both cell proliferation and telomerase activity to a certain extent. Without exception, none of these 17 sesquiterpenes could only inhibit telomerase activity without inhibiting cell proliferation. This indicated that the telomerase inhibiting activity is not a universal mechanism for all anticancer drugs but is only one of several possible mechanisms. The structure-activity relationships of 5 groups of sesquiterpenes are also discussed. This study may help to develop anticancer drugs.
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PMID:The effect of 17 sesquiterpenes on cell viability and telomerase activity in the human ovarian cancer cell line HO-8910. 1729 83

A thiaether metal complex 1-aza-4,7-dithiacyclononane-RhCl3, 2, and cyclic amine metal complexes tacn-CuBr2, 3, and Me3tacn-RuCl3, 4, have been evaluated for anticancer activity against the ovarian cancer cell line NuTu-19 and for cell toxicity against the noncancerous ovarian tissue cell line OVepi. Specifically, metal complex 2 is active when compared to cisplatin at micromolar concentrations using the MTT and cell invasion assay. The in vitro results reported warrant further evaluation of metal complex 2 in living systems.
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PMID:Ovarian cancer activity of cyclic amine and thiaether metal complexes. 1734 69

To explore the role and possible mechanism of apoptosis and caspase-3 activity in the development of multicellular drug resistance of ovary cancer. Ovarian cancer cell A2780 multicellular spheroids (MCS) were obtained from three-dimensional culture. Drug sensitivity of monolayer cells (MC) and MCS were respectively tested by MTT staining and cytometry. The apoptosis of MC and MCS were determined by the flow cytometry (FCM). The expression of bcl-2 and caspase-3 in A2780/MC and A2780/MCS were detected by using Western blot and caspase-3 assay kit. A2780/MC was compacted into mass after 2 days in three-dimensional cell culture model, and MCS had more than two layers of cells growing within 5 days. Compared with A2780/MC, A2780/MCS were more resistant to the anticancer drug, and the apoptosis rate was significantly lower than those of A2780/MC. The activity of caspase-3 in A2780/MCS was significantly lower than the A2780/MC. But the expression of bcl-2 in A2780/MCS was significantly higher than that in A2780/MC. It was suggested that the drug resistance of MCS might be associated with the overexpression of anti-apoptosis protein bcl-2 and the down-regulation of caspase-3 activity.
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PMID:Construction of three-dimensional in vitro culture model of ovarian carcinoma and the study of its multicellular drug resistance. 1735 6

Paclitaxel (taxol) is extensively used for chemotherapy of various cancers including ovarian cancer. Although paclitaxel induces apoptosis in cancer cells, its exact mechanism of action still remains to be determined. Akt mediates survival signals which preserve various cancer cells from apoptosis pathway. Thus, Akt is considered an exciting target for therapeutics. Here, we demonstrated that inhibition of Akt increases the efficacy of the paclitaxel-induced apoptosis in SKOV3 and PA-1 human ovarian cancer cells. The sensitivity to paclitaxel of SKOV3 and PA-1 cells was examined using the MTT assay. At a concentration of 30 nM, PA-1 cells were more sensitive to paclitaxel than SKOV3 cells. Apoptosis was accompanied by the release of cytochrome c into the cytoplasm and cleavage of poly (ADP-ribose) polymerase (PARP). To further elucidate the mechanism of apoptosis by paclitaxel, we compared the levels of phosphorylation of Akt between paclitaxel-resistant SKOV3 cells and paclitaxel-sensitive PA-1 cells. The higher level of phosphorylated Akt was shown in SKOV3 cells than in PA-1 cells. Interestingly, the treatment of paclitaxel decreased the amount of phosphorylated Akt in a time-dependent manner in both cell lines. Furthermore, inhibition of Akt by specific phosphatidyinositol-3-kinase (PI3K)-Akt inhibitors (Wortmannin, and LY294002) synergistically increased the efficacy of the paclitaxel-induced apoptosis in both cell lines. These results suggest that the addition of the Akt inhibitor may increase the therapeutic efficacy of paclitaxel for patients with ovarian cancer.
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PMID:Akt involvement in paclitaxel chemoresistance of human ovarian cancer cells. 1740 21


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