河北医科大学学报

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ATIP3aHMGA2ERK信号通路对卵巢上皮细胞癌顺铂耐药性的影响

  

  1. 河北省沧州市中心医院妇一科,河北 沧州 061000
  • 出版日期:2018-10-25 发布日期:2018-09-27
  • 作者简介:黄平(1978-),女,河北沧州人,河北省沧州市中心医院主治医师,医学硕士,从事妇科疾病诊治研究。

Effects of ATIP3aHMGA2ERK signaling pathway on cisplatin resistance in epithelial ovarian cancer

  1. The First Department of Gynaecology, Cangzhou Central Hospital, Hebei Province, Cangzhou 061000, China
  • Online:2018-10-25 Published:2018-09-27

摘要: [摘要]〓
〖HTH〗目的〖HTSS〗〖KG*2〗探讨血管紧张素Ⅱ受体的相互作用蛋白3a(angiotensin Ⅱ type 2 receptorinteracting protein 3a,ATIP3a)-高迁移率族蛋白A2(high mobility group AThook 2,HMGA2)-细胞外调节蛋白激酶(extracellular regulated protein kinase,ERK)信号通路对卵巢上皮细胞癌顺铂耐药性的影响。
〖HTH〗方法〖HTSS〗〖KG*2〗培养顺铂耐药卵巢癌细胞株SKOV3/DDP、A2780/DDP,分为8组(n=3),对照组C1和C2组仅向SKOV3/DDP、A2780/DDP细胞中加入RMPI 1640培养基,A1组和A2组为分别向SKOV3/DDP、A2780/DDP细胞中加入ATIP3a多肽(1 nmol/L)处理6 h,S1和S2组为分别向SKOV3/DDP、A2780/DDP细胞中转染siRNAATIP3a,VC1和VC2组分别向SKOV3/DDP、A2780/DDP细胞中转染siRNAvector作为对照。顺铂3 μg/mL处理72 h后,采用乳酸脱氢酶法检测细胞的增殖能力,体外侵袭实验检测细胞侵袭能力,Realtime PCR法检测HMGA2 mRNA表达,免疫蛋白印记法检测HMGA2和磷酸化ERK的表达。
〖HTH〗结果〖HTSS〗〖KG*2〗A1组SKOV3/DDP细胞增殖率和侵袭能力、HMGA2 mRNA和蛋白表达、磷酸化ERK蛋白表达明显低于C1组,S1组SKOV3/DDP细胞增殖率和侵袭能力、HMGA2 mRNA和蛋白表达、磷酸化ERK蛋白表达明显高于C1组、A1组,VC1组SKOV3/DDP细胞增殖率和侵袭能力、HMGA2 mRNA和蛋白表达、磷酸化ERK蛋白表达高于A1组,低于S1组,差异均有统计学意义(P<005); A2组A2780/DDP细胞增殖率和侵袭能力、HMGA2 mRNA和蛋白表达、磷酸化ERK蛋白表达低于C2组; S2组A2780/DDP细胞增殖率和侵袭能力、HMGA2 mRNA和蛋白表达、磷酸化ERK蛋白表达明显高于C2组、A2组,VC2组A2780/DDP细胞增殖率和侵袭能力、HMGA2 mRNA和蛋白表达、磷酸化ERK蛋白表达高于A2组,低于S2组,差异均有统计学意义(P<005)。
〖HTH〗结论〖HTSS〗〖KG*2〗卵巢上皮细胞癌顺铂耐药性可能与ATIP3aHMGA2ERK信号通路有关。

关键词: 卵巢肿瘤, 顺铂耐药性, ATIP3aHMGA2ERK信号通路

Abstract: [Abstract] Objective〖HTSS〗〓To explore the effects of ATIP3aHMGA2ERK signaling pathway on cisplatin resistance in epithelial ovarian cancer.
〖HTH〗〖WTHZ〗Methods〖HTSS〗〓DDPresistant ovarian cancer cell lines SKOV3/DDP and A2780/DDP were cultured to exponential phase and assigned to control group(C1and C2 Group), ATIP3a group(A1 and A2 Group), siRNAATIP3a group(S1and S2 Group) and siRNAvector group(VC1 and VC2 Group)(n=3), respectively. The cells in A1 and A2 groups were treated with ATIP3a polypeptides(1 nmol/L). The cells in S1 and S2 groups were treated with siRNAATIP3a, but VC1 and VC2 were treated with siRNAvector as control. Then all the cells were treated with DDP for 72 h. The effects of cell proliferation and invasion were assessed by lactate dehydrogenase and transwell assays. The expression in HMGA2 was measured by Realtime PCR and westernblot. Phosphorylation of ERK was also assessed by Westernblot.
〖HTH〗〖WTHZ〗Results〖HTSS〗〓Compared with C1, ATIP3a polypeptides treatment decreased cell proliferation,invasion, mRNA and protein expression of HMGA2, and phosphorylation of ERK in A1 group. Compared with C1 and A1 groups, siRNAATIP3a increased cell proliferation, invasion, mRNA and protein expression of HMGA2, and phosphorylation of ERK in S1 group. The cell proliferation, invasion, mRNA and protein expression of HMGA2, and phosphorylation of ERK in VC1 group were increased compared with A1, but decreased compared with S1. Compared with C2, ATIP3a polypeptides treatment decreased cell proliferation, invasion, mRNA and protein expression of HMGA2, and phosphorylation of ERK in A1 group. Compared with C2 and A2 groups, siRNAATIP3a increased cell proliferation, invasion, mRNA and protein expression of HMGA2, and phosphorylation of ERK in S2 group.The cell proliferation, invasion, HMGA2 expression of mRNA and protein, and phosphorylation of ERK in VC2 group were increased compared with A2, but decreased compared with S2.
〖HTH〗〖WTHZ〗Conclusion〖HTSS〗〓The DDPresistant of human epithelial ovarian cancer might be associated with ATIP3aHMGA2ERK signal pathway.

Key words: ovarian neoplasms, cisplatin resistance, ATIP3aHMGA2ERK signal pathway