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首页|期刊导航|现代妇产科进展|RNAi介导的WFDC2基因沉默抑制人卵巢浆液性上皮癌生长的体内实验

RNAi介导的WFDC2基因沉默抑制人卵巢浆液性上皮癌生长的体内实验

朱亚飞 高国兰 褚芳

现代妇产科进展2016,Vol.25Issue(3):187-191,5.
现代妇产科进展2016,Vol.25Issue(3):187-191,5.DOI:10.13283/j.cnki.xdfckjz.2016.03.031

RNAi介导的WFDC2基因沉默抑制人卵巢浆液性上皮癌生长的体内实验

The role and mechanism of RNAi-mediated silencing of WFDC2 in the progression of human serous epithelial ovarian cancer in vivo study

朱亚飞 1高国兰 2褚芳3

作者信息

  • 1. 赣南医学院第一附属医院妇产科,赣州 341000
  • 2. 中国医科大学航空总医院妇产科
  • 3. 中国科学院北京转化医学研究院,北京 100012
  • 折叠

摘要

Abstract

Objective:To establish subcutaneous transplanted model of human ovarian carcinoma in nude mice with cell lines with stablely lentiviral WFDC2 gene sequence of small interfering siRNA and to explore its influence on tumor growth and metastasis. Methods:Sub-group was labeled by OEC ( ovarian epithelial cancinoma cell lines) ,OEC-mock( transfected by mock lentiviral vector ) and OEC-WFDC2-si ( transfected by with stablely lentiviral WFDC2 gene sequence of small interfering siRNA) . Tumor volume were detected by continuous meas-urement to draw the tumor growth curve. Tumor volume and weight were measured at the end point of the study,proliferating cell nuclear antigen( PCNA) was detected by immunohistochem-istry ( IHC) . Results:The growth rate was slower and time for first visible tumors was earlier for WFDC silencing group (P<0. 05),tumor weight,volume and PCNA were lower in WFDC2 si-lencing group than control group, no metastasis was found in any group. Conclusions:It has been confirmed that WFDC2 gene silencing significantly inhibit the growth of ovarian cancer. WFDC2 gene plays a key role in ovarian cancer development involved in regulating the tumor proliferation.

关键词

WFDC2基因/人附睾蛋白4/卵巢癌

Key words

WFDC2/Human epididymal secretory protein 4/Ovarian neoplasms

分类

医药卫生

引用本文复制引用

朱亚飞,高国兰,褚芳..RNAi介导的WFDC2基因沉默抑制人卵巢浆液性上皮癌生长的体内实验[J].现代妇产科进展,2016,25(3):187-191,5.

基金项目

江西省教育厅基金(No:GJJ14675) (No:GJJ14675)

赣南医学院科研项目(No:YB201301) (No:YB201301)

赣南医学院重点科研项目(No:ZD201404) (No:ZD201404)

现代妇产科进展

OA北大核心CSCDCSTPCD

1004-7379

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