Objective To investigate N-myc downstream-regulated gene 2(NDRG2) expression in ovarian cancer cells and its potential usefulness as a diagnostic marker and/or target for therapeutic intervention.Methods Human NDRG2 L...Objective To investigate N-myc downstream-regulated gene 2(NDRG2) expression in ovarian cancer cells and its potential usefulness as a diagnostic marker and/or target for therapeutic intervention.Methods Human NDRG2 L/S gene was obtained by revers-transcription polymerase chain reaction(RT-PCR). Sequence analysis confirmed the identity of NDRG2 L/S gene, which was then inserted into a eukaryotic vector p LNCX2, which was in turn transfected into NDRG2 gene-negative HO-8910 cells. Flow cytometry(FCM) and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT) assay were conducted to determine the proliferation rate of HO-8910 cells. Cisplatin resistance of HO-8910 cells transfected with p LNCX2-NDRG2 L/S was evaluated by FCM. Tumors were generated in female nude mice by subcutaneous injection of HO-8910 cells.Results NDRG2 gene was isolated and its expression vector was successfully constructed. NDRG2 expression positively correlated with the proliferation of HO-8910 cells. NDRG2 L/S promoted tumorigenicity in HO-8910 cells.Conclusion The present study identified a novel function of NDRG2 L/S gene and demonstrated its involvement in the promotion of ovarian cancer cell proliferation and enhancement of cisplatin resistance in HO-8910 cells. Future studies are warranted to determine the relationship between NDRG2 upregulation and ovarian cancer progression.展开更多
Objective： The aim of the study was to investigate the mechanism of gemcitabine （GEM） combination with radiation on the high metastasis human ovarian cancer cell line （HO-8910PM）. Methods： Human ovarian cancer c...Objective： The aim of the study was to investigate the mechanism of gemcitabine （GEM） combination with radiation on the high metastasis human ovarian cancer cell line （HO-8910PM）. Methods： Human ovarian cancer cell line HO- 8910PM was treated with different concentrations of gemcitabine for 24 h, then the cells were counted. In the study of GEM combination with radiation, an efficiency of colony formation was observed; the cell cycle and apoptosis were analyzed by flow cytometry; the experiment of depend on the time and its radio sensitivity were observed by using mitotic index with the cells for each 24, 48, 72 and 96 h after experiment. Results： It suggested that the GEM had an inhibition effect on the human ovarian cancer cell line. The alive cell numbers were decreased by following a height of GEM concentration. When GEM in combina- tion with a radiation, the suppression was significantly increased than that of single GEM therapy. The efficiency of colony formation was significantly lower, under this condition the cell could be arrested at G0-G1 phase and could be decreased to enter into the S phase; the apoptosis percentage could be significantly increased; especially, under the 4 Gy and 6 Gy doses the cell apoptosis was more obvious. GEM combination with radiation had depended on the time to the cells; mitotic index of the calls in combination group was observed significantly lower than that of single GEM therapy or single radiation, and this showed that it had an effect of radiosensitivity. Conclusion： The GEM has a significant growth inhibition on the human ovarian cancer cells, GEM combination with radiation could induce HO-8910PM cell occurred arrested and apoptosis. It has depended on the time and has a radiosensitivity effect. The result shows that it is a better method to treat the human ovarian cancer by using radiotherapy combined with gemcitabine.展开更多
文摘Objective To investigate N-myc downstream-regulated gene 2(NDRG2) expression in ovarian cancer cells and its potential usefulness as a diagnostic marker and/or target for therapeutic intervention.Methods Human NDRG2 L/S gene was obtained by revers-transcription polymerase chain reaction(RT-PCR). Sequence analysis confirmed the identity of NDRG2 L/S gene, which was then inserted into a eukaryotic vector p LNCX2, which was in turn transfected into NDRG2 gene-negative HO-8910 cells. Flow cytometry(FCM) and 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide(MTT) assay were conducted to determine the proliferation rate of HO-8910 cells. Cisplatin resistance of HO-8910 cells transfected with p LNCX2-NDRG2 L/S was evaluated by FCM. Tumors were generated in female nude mice by subcutaneous injection of HO-8910 cells.Results NDRG2 gene was isolated and its expression vector was successfully constructed. NDRG2 expression positively correlated with the proliferation of HO-8910 cells. NDRG2 L/S promoted tumorigenicity in HO-8910 cells.Conclusion The present study identified a novel function of NDRG2 L/S gene and demonstrated its involvement in the promotion of ovarian cancer cell proliferation and enhancement of cisplatin resistance in HO-8910 cells. Future studies are warranted to determine the relationship between NDRG2 upregulation and ovarian cancer progression.
文摘Objective： The aim of the study was to investigate the mechanism of gemcitabine （GEM） combination with radiation on the high metastasis human ovarian cancer cell line （HO-8910PM）. Methods： Human ovarian cancer cell line HO- 8910PM was treated with different concentrations of gemcitabine for 24 h, then the cells were counted. In the study of GEM combination with radiation, an efficiency of colony formation was observed; the cell cycle and apoptosis were analyzed by flow cytometry; the experiment of depend on the time and its radio sensitivity were observed by using mitotic index with the cells for each 24, 48, 72 and 96 h after experiment. Results： It suggested that the GEM had an inhibition effect on the human ovarian cancer cell line. The alive cell numbers were decreased by following a height of GEM concentration. When GEM in combina- tion with a radiation, the suppression was significantly increased than that of single GEM therapy. The efficiency of colony formation was significantly lower, under this condition the cell could be arrested at G0-G1 phase and could be decreased to enter into the S phase; the apoptosis percentage could be significantly increased; especially, under the 4 Gy and 6 Gy doses the cell apoptosis was more obvious. GEM combination with radiation had depended on the time to the cells; mitotic index of the calls in combination group was observed significantly lower than that of single GEM therapy or single radiation, and this showed that it had an effect of radiosensitivity. Conclusion： The GEM has a significant growth inhibition on the human ovarian cancer cells, GEM combination with radiation could induce HO-8910PM cell occurred arrested and apoptosis. It has depended on the time and has a radiosensitivity effect. The result shows that it is a better method to treat the human ovarian cancer by using radiotherapy combined with gemcitabine.
