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Correlation With Ovarian Ascites And Chemoresistance In Ovarian Cancer

Posted on:2017-06-11Degree:MasterType:Thesis
Country:ChinaCandidate:P LiuFull Text:PDF
GTID:2334330509962071Subject:Oncology
Abstract/Summary:PDF Full Text Request
Objectives: Ovarian cancer mortality is highest in gynecologic malignancies. The standard treatment of ovarian cancer is ideal cytoreductive surgery and neoadjuvant chemotherapy based on platinum and paclitaxel after surgery. Although there has great progress in the treatment, the relapse or metastasis of the disease will eventually happen. The main reason for this lies in chemo-resistance. How to predict drug resistance and guide treatment in ovarian cancer has become a hot issue. Advanced ovarian cancer patients are often accompanied by the malignant ascites, and the cytokine in ascites is closely related to progression-free survival and prognosis of cancer patients. In addition, ovarian ascites can promote tumor cell proliferation and inhibit apoptosis. Thus, we hypothesized that ovarian cancer ascites may promote the occurrence of ovarian cancer drug resistance. Therefore, in this study, we firstly detect the ascites how to influent the biological behavior of ovarian cancer cells, and then explore the correlation between ascites and chemoresistance.Methods: 1. To collect 23 cases of ovarian cancer ascites supernatant, and use them to culture ovarian cancer SKOV3 cells. The cells were divided into experimental groups(ascites culture group) and control group according to the culture conditions. 2. MTT assay, wound scratch assay and transwell were used to investigate the effect of ascites on the ability of proliferation, migration and invasion of SKOV3. 3. Treatment of different concentrations of chemotherapeutic drugs in the experimental group and the control group. MTT method was used to describe ovarian cancer SKOV3 cells, cells treated with ascites and ascites tumor cells sensitivity of paclitaxel. 4. Flow cytometry was used to detect the apoptosis of SKOV3 cells in different groups after chemotherapy drugs treatment. 5. Western Blot was used to detect the expression levels of resistance protein in control group, cells treated with ascites group and ascites tumor cells group.Results: 1. MTT assay and wound healing assay showed that ascites can promote the proliferation and migration of ovarian cancer SKOV3 cells(P<0.05). Transwell assay showed that, compared with SKOV3 blank control group, there was no significant difference in the cell number in cells treated with ascites group(P>0.05), and ascites did not increase the invasion ability of SKOV3 cells. 2. MTT method was used to detect the sensitivity of the cells in the ascites tumor cell group, the ascites culture group and the control group to the chemotherapy drug paclitaxel. The results showed that, in the same drug concentration, the cell inhibition rate of ascites tumor cells and ascites group was significantly lower than that of the control group, while the ascites tumor cell group was significantly lower than that of the ascites group. After treatment of ascites, the sensitivity of SKOV3 cells to paclitaxel was significantly decreased(P<0.05), which decreased by about 2.3 times compared with the control group. 3. Flow cytometry assay showed that, compared with the control group, cell apoptosis rate of the ascites culture group had no significant change(P > 0.05); After the effect of paclitaxel on 24 h, the apoptosis rate of the ascites culture group was significantly lower than that of the control group(P<0.05). 4. Ovarian cancer ascites can increase the expression of multidrug resistance protein of SKOV3 cells and tumor cells in ascites.Conclusions: 1. Ovarian cancer ascites can promote the proliferation and migration of ovarian cancer SKOV3 cells. 2. Ovarian cancer ascites increased the resistance of ovarian cancer SKOV3 cells to paclitaxel and reduced cell apoptosis. 3. Ovarian cancer ascites can increase the expression of drug resistance protein in tumor cells.
Keywords/Search Tags:Ascites, Ovarian carcinoma, Drug resistance, Resistance protein, Paclitaxel
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