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Objective To study the effect on ovarian tumor migration invasion after inhibition the expression of IGFBP2, IGFBP3.Methods siRAN interference IGFBP2, IGFBP3 expression in ovarian cancer cell lines SKOV3, SKOV3 proliferation detected by CCK-8 kits,SKOV3 apoptosis detected by flow cytometry ,SKOV3 migration and invasion detected by transwell experiment and scratched cell healing detection; CCK-8 method detected survival after treated different concentrations of cisplatin (5, 10, 15, 20 ug/mL).Results The proliferation ability of SKOV3 dropped and apoptosis increased after treated siRAN IGFBP 2, IGFBP3 compared with the control group , migration and invasion function decline, resistance level to improve greatly.Conclusions The expression of IGFBP2, IGFBP3 in ovarian cancer affected migration and invasion .
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Objective:To study the change ofTIZ expression in epithelial ovarian cancer cells.Methods:HO8910 cells were transinfected with siRNA to inhibit the expression ofTIZ. pcDNA3.1-TIZ vectors were combined to increase theTIZ expression level.The cell viability, colony forming efficiency and cycle distribution ofHO8910,HO8910/NC,HO8910/pcDNA3.1-NC,HO8910/TIZ-573 andHO8910/pcDNA3.1-TIZ were compared, and the invasion rate, migration rate and adhesion rate between5 groups of cells were compared.Results:Compared with those ofHO8910,HO8910/NC andHO8910/pcDNA3.1-NC, the cell viability, colony forming efficiency and cell cycle distribution ofHO8910/TIZ-573 were increased, while the indexes ofHO8910/pcDNA3.1-NC were decreased with statistical significant difference(P0.05). Conclusions:The expression ofTIZ can inhibit the proliferation of epithelial ovarian cancer cells.
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Objective To discuss the clinical effect of neoadjuvant chemotherapy combined tumor cells to destroy the loss in treatment of patients with advanced ovarian cancer.Methods One hundred and forty-four patients with advanced ovarian cancer were divided randomly into the control group(n=72) and research group (n=72).The patients of control group were given conventional chemotherapy(ovarian tumor remove first and then neoadjuvant chemotherapy) and the patients of research group were given neoadjuvant chemotherapy (neoadjuvant chemotherapy first and then ovarian tumor remove).The operation time, intraoperative blood loss, hospital stay, ideal reduction rate, clinical efficacy and postoperative complications between the two groups were compared.Results The operation time, intraoperative blood loss, hospital stay of the research group were obviously lower than that of the control group((124.6±21.3) min vs.(186.4±32.6) min, (382.5±62.3) ml vs.(618.5± 86.4) ml, (8.9± 1.3) d vs.(12.2± 3.4) d;t =5.623,9.646,5.257), while the ideal reduction rate of the research group were obviously higher than that of the control group(70.8％ vs.47.2％, x2 =8.735), the differences were statistically significant(P＜0.05).The clinical efficacy(87.5％ vs.52.8％, x2 =6.748) of the research group were obviously higher than that of the control group, while the postoperative incision infection (9.7％ vs.19.4％, x2 =4.452) and fever(4.2％ vs.15.3％,x2 =5.536) were obviously lower than that of the control group, the differences were statistically significant (P＜0.05).Conclusion The treatment of neoadjuvant chemotherapy can obviously increase the the clinical effect of treatment of patients with advanced ovarian cancer and decrease the postoperative complications, it is worth popularization and application.
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Objective To construct adenovirus vector with agiostatinK1-5 gene and to investigate the function of suppression to proliferation and migration for vascular endothelial cells.Methods With the use of gene recombination and clone technology, we constructed the adenovirus vector with the gene of angiostatin K1-5. In vitro vascular endothelial eclls proliferation assay and migration activity were performed through direct infection,MTT and transwell chemotaxis assay. Results 50% TCID indicated that the condence of resultant viruses was 1.5?109PFU/mL. It was purified by CsCL banding,final yield were generally 1.1?1010 PFU/mL plaquing-forming units. Through indirect infect assay and MTT, we found angiostatin K1-5 inhibited human vascular endothelial cells proliferation. We utilized human vascular endothelial cells to study the effect angiostatin K1-5 on cell migration,the result showed that adenoviruse vector with angiostatin K1-5 significantly inhibited HUVEC migration.Conclusion We successfully constructed adenoviruse vector with angiostatin K1-5 and demonstrated its inhibitory effect on proliferation andmigration of HUVEC.