文章摘要
范进锋,陈松强,马 哲,李 琦,周治彦,金应霞,梁培育,李浩勇.shRNA抑制活化诱导的胞苷脱氨酶(AID)对前列腺癌细胞C4-2表型的影响[J].,2019,19(16):3062-3067
shRNA抑制活化诱导的胞苷脱氨酶(AID)对前列腺癌细胞C4-2表型的影响
Effects of shRNA Inhibition of Activation of Cytidine Deaminase (AID) on the Phenotype of Prostate Cancer Cell Line C4-2
投稿时间:2018-12-06  修订日期:2018-12-30
DOI:10.13241/j.cnki.pmb.2019.16.011
中文关键词: 活化诱导的胞苷脱氨酶(AID)  RNA干扰技术(RNAi)  前列腺癌  增殖  凋亡  迁移  侵袭
英文关键词: Activation-induced cytidine deaminase (AID)  RNA interference (RNAi)  Prostate cancer  Proliferation  Apoptosis  Migration  Invasion
基金项目:海南省自然科学基金项目(20158298);国家自然科学基金项目(81360357);海南省社会发展重大专项课题(2015SF31)
作者单位E-mail
范进锋 海南医学院第一附属医院泌尿外科 海南 海口570102 769963801@qq.com 
陈松强 海南医学院第一附属医院泌尿外科 海南 海口570102  
马 哲 海南医学院第一附属医院泌尿外科 海南 海口570102  
李 琦 1 海南医学院第一附属医院泌尿外科 海南 海口5701022武汉大学人民医院泌尿外科 湖北 武汉 430060  
周治彦 海南医学院第一附属医院泌尿外科 海南 海口570102  
金应霞 武汉大学第一临床学院中心实验室 湖北 武汉 430060  
梁培育 海南医学院第一附属医院泌尿外科 海南 海口570102  
李浩勇 1 海南医学院第一附属医院泌尿外科 海南 海口5701022武汉大学人民医院泌尿外科 湖北 武汉 430060  
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中文摘要:
      摘要 目的:探讨AID在前列腺癌中的表达情况,AID对前列腺癌细胞C4-2的侵袭、迁移、增殖以及凋亡方面的影响。方法:应用靶向敲减AID的慢病毒对前列腺癌细胞C4-2进行干扰,运用Western-blot、免疫组化、平板克隆形成、流式、Transwell实验对前列腺癌组织和前列腺癌细胞C4-2表型的变化情况进行研究。结果:临床前列腺癌样本中AID高表达,良性前列腺增生组织中AID低表达,正常前列腺组织不表达(*P<0.05); shRNA干扰以后的shAICDA-C4-2单克隆细胞株中AID的表达量显著降低,其增殖、迁移和侵袭能力阳性对照组(Monoclonal6)与阴性对照组(NC)相比分别降低49%、80%、63%,凋亡率阳性对照组(Monoclonal6)为阴性对照组(NC)的3.2倍。结论:前列腺癌组织中AID高表达,AID在促进前列腺癌细胞的增殖、迁移、侵袭,抑制前列腺自细胞的凋亡中具有极其重要的作用。AID表达极可能与前列腺癌的进展、预后明显相关。
英文摘要:
      ABSTRACT Objective: To investigate the expression of AID in prostate cancer and the effect of targeted knockdown on invasion, migration, proliferation and apoptosis of prostate cancer cell line C4-2. Methods: Using a lentivirus targeting knockdown of AID to interfere with prostate cancer cell line C4-2; western-blot, immunohistochemistry, flow cytometry and transwell assay were used to study the expression of AID in prostate tissue and the changes of the phenotype of prostate cancer cell line C4-2. Results: The relative expression level of AID in clinical prostate cancer samples was 9.02±1.85, which was significantly higher than that in benign prostatic hyperplasia tissues 1.89±0.45, and normal prostate tissues were not expressed (*P<0.05); the expression of AID in the shAICDA-C4-2 monoclonal cell line was significantlydecreased after shRNA interference, and the positive control group (Monoclonal6) with proliferation, migration and invasion ability decreased by 49%, 80%, 63%, respectively, compared with the negative control group (NC), and the apoptotic rate of positive control group (Monoclonal6) was 3.2 times that of negative control group (NC). Conclusion: High expression of AID in prostate cancer tissues, AID plays an extremely important role in promoting the proliferation, migration and invision of prostate cancer cells and inhibiting the apoptosis of prostate cancer cells. Therefore, its expression highly likely to be significantly associated with the progression and prognosis of prostate cancer.
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