The Effects Of Etoposide Combined With Cisplatin On Killing Skov₃ Ovarian Cancer Cells

Objective: Ovarian carcinoma is one of the commonlyseen malignant tumors what originated reproductive organ offemale. It is very late when the ovarian carcinoma was beendiscovered because of lacking the effective diagnostic methods.So the mortality rate of ovarian carcinoma is the first one in themalignant tumor of gynecology and the subsist rate in 5 years ispercent of thirty, which is very low. Operation is the mainmethod for the patients of ovarian carcinoma. But it is the mostimportant way that we use multiple methods such aschemotherapy, radiotherapy…etc. Among these treatments,many courses of chemotherapy is very important. It issignificant for those patients of ovarian carcinoma in laterperiod.There are some reasons for our clinical doctors must to findan effective plan of chemotherapy. Firstly: it is very late whenthe ovarian carcinoma was discovered and even some caseshave no chance to go to operate. Secondly: the rate ofrecurrence which cases were treated by operation orchemotherapy is very high. In addition, it is easy for the cell ofovarian carcinoma to emerge the resistance during the coursesof chemotherapy. To sum up, it is significant for clinicaldoctors to find a most effective plan of chemotherapy.At present,almost doctors choose cisplatin (CDDP) as thefirst choosing drugs; meanwhile, they choose some other drugsas the compatibility. Among these compatibility drugs ,topoisomeraseII inhibitor is often used, such as etoposide(VP-16),adriamycin,novobiocin…etc. DNA topoisomeraseIIis a ubiquitous enzyme that is essential for survival of theeukaryotic organisms, playing an important role in mostprocesses of the DNA mechanisms. In this study, our objectiveis to evaluate the effects of topoisomeraseII inhibitor (VP-16) oninhibiting the SKOV3 cells'developing. we investigate theeffects of VP-16combined with CDDP and CDDP single usedon killing of ovarian cancer cells, the microculture tetrazolium(MTT) assay was used to determine the inhibition rates ofVP-16 in peak serum concentration combined with differentconcentration of CDDP , or CDDP on SKOV3 cells ,respectively.Methods: 1 The cells series serous cystadenocarcinomaof ovary (SKOV3) that we buy them from the people's hospitalof Beijing university.2 we use 1640 culture medium to cultivate SKOV₃ cellsunder the surroundings of the temperature is 37℃, theconcentration of CO₂ is 5%.3 According to the peak serum concentration (psc), wedivided these cells into six groups. We dealed with the firstgroup cells by 1/10 psc of CDDP (0.3μg/ml) single. The secondgroup cells were dealed with by one times psc of CDDP (3μg/ml)only. The third were dealed with by ten times psc of CDDP(30μg/ml).The other three groups cells were dealed with byVP-16 which in psc combined with different concentration ofCDDP(1/10 psc, psc, 10psc), respectively.4 After dealed with these groups of cells, we used themicroculture tetrazolium (MTT) assay to determine theinhibition rates of VP-16 in peak serum concentration combinedwith different concentration of CDDP, or CDDP on SKOV₃cells in different times:0h, 8h, 16h, 24h, respectively. Thecombination efficiency of the drugs was analyzed by statisticsfrom the MTT results.5 According to the peak serum concentration (psc), Wedivided cells into six groups similarly. After us dealed with thesecells,immunocytochemical analysis was performed to revealedTopoII αand TopoII βexpressions of all of six groups'cells. Weobserved the expression of TopoII αand TopoII βin the cellsnuclear and counted the number of positive cell nuclear undermicroscope after performing immunohistochemical staining.Results: 1 the inhibition rates of all of groups after thecells were treated with 0h: VP-16 could enhance the effect ofCDDP on SKOV3 cells. The inhibition rates were (2.5±0.2),(3.2±0.7) and (9.3±1.1), respectively following treatment with0.3 , 3 , 30μg/ml of CDDP. When combined withVP-16(5μg/ml), the inhibition rates raised to (4.4±0.2),(5.9±0.8) and (6.2±0.7), respectively. The value of Q was0.86(+), 0.99(+) and 1.08(+) when treated with 0.3, 3,30μg/ml CDDP which combined with VP-16(5μg/ml) ,respectively.2 the inhibition rates of all of groups after the cells weretreated with 8h: VP-16 could enhance the effect of CDDP onSKOV₃ cells. The inhibition rates were (5.6±0.3), (17.2±1.2)and (40.4±2.1), respectively following treatment with 0.3, 3,30μg/ml of CDDP. When combined with VP-16(5μg/ml), theinhibition rates raised to (24.4±1.6) , (37.9±2.8) and(52.3±4.1), respectively. The value of Q was 0.89(+), 1.03(+)and 1.12(+) when treated with 0.3, 3, 30μg/ml CDDP whichcombined with VP-16(5μg/ml), respectively.3 the inhibition rates of all of groups after the cells weretreated with 16h: VP-16 could enhance the effect of CDDP onSKOV3 cells. The inhibition rates were (6.5±0.6), (19.2±1.7)and (49.3±2.5), respectively following treatment with 0.3, 3,30μg/ml of CDDP. When combined with VP-16(5μg/ml), theinhibition rates raised to (31.4±4.2) , (42.9±3.8) and(61.2±5.1), respectively. The value of Q was 0.96(+), 1.09(+)and 1.38(++) when treated with 0.3, 3, 30μg/ml CDDP whichcombined with VP-16(5μg/ml), respectively.4 the inhibition rates of all of groups after the cells weretreated with 24h: VP-16 could enhance the effect of CDDP onSKOV₃ cells. The inhibition rates were (6.9±0.5), (21.4±1.9)and (52.4±4.3), respectively following treatment with 0.3, 3,30μg/ml of CDDP. When combined with VP-16(5μg/ml), the...