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作 者:王小萼[1] 汪宏波[1] 王泽华[1] 张靖[1] 徐媛[1] 徐亚辉[1] 汪茜[1]
机构地区:[1]华中科技大学同济医学院附属协和医院妇产科,武汉430022
出 处:《现代妇产科进展》2009年第10期739-742,共4页Progress in Obstetrics and Gynecology
摘 要:目的:探讨酪氨酸激酶受体B(TrkB)对上皮性卵巢癌细胞失巢凋亡的影响,以寻求治疗卵巢癌的新靶点。方法:用RT-PCR法检测TrkB在上皮性卵巢癌细胞株CAOV3中的表达;MTT法检测激活和抑制TrkB对细胞增殖的影响;用poly-hema和琼脂构建两种失巢环境,流式细胞仪检测BDNF和酶抑制剂K252-a作用TrkB后细胞失巢凋亡和集落形成情况。结果:TrkB在CAOV3细胞株上明显表达。BDNF激活TrkB可使CAOV3细胞增殖增强,增强细胞抗失巢凋亡能力和集落形成能力。K252-a抑制TrkB后可降低细胞抗失巢凋亡能力和集落形成能力,差异有统计学意义(P<0.01)。结论:上皮性卵巢癌抗失巢凋亡能力与TrkB/BDNF作用通路有关,激活TrkB可增强CAOV3抗失巢凋亡能力,可能为卵巢癌靶向治疗提供新途径。Objective :To investigate the effects of tyrosine kinase receptor B (TrkB) on anoikis of ovarian cancer cell in vitro. Methods : TrkB expression of the human ovarian cancer CAOV3 cell was analyzed by RT-PCR. The proliferation of cell line was examined with 3-(4,5- dirnethyhhiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTF) assay. The effect of TrkB on anoikis resistance of ovarian cancer cell line was detected by clone formation test and by flow cytometry(FCM) in Suspension culture system. Results:The expression of TrkB was obtained in CAOV3 cell;TrkB activated by BDNF could improve the proliferation,anoikis resistance and the clone formation of CAOV3 cell. In contrast, the inhibition of TrkB by addition of K252-a could increased cell anoikis and decreased the clone formation (P〈0.01). Conclusion: TrkB/BDNF is probably one of the important pathway on ovarian cancer cell's resistance to anoikis. Activated TrkB can improve the capability of anoikis resistance of ovarian cancer. This may be a new thera- peutic target of ovarian cancer in clinical application in future.
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