• 中国科学论文统计源期刊
  • 中国科技核心期刊
  • 美国化学文摘(CA)来源期刊
  • 日本科学技术振兴机构数据库(JST)

临床输血与检验 ›› 2022, Vol. 24 ›› Issue (5): 574-581.DOI: 10.3969/j.issn.1671-2587.2022.05.005

• 基础研究 • 上一篇    下一篇

lncRNAs ABHD11-AS1靶向miR-133a上调EGFR表达促进卵巢癌细胞增殖*

王之丰, 孙昊, 胡电, 金志军, 刘晓军   

  1. 200003 海军军医大学第二附属医院妇产科
  • 收稿日期:2021-11-26 出版日期:2022-10-20 发布日期:2022-10-31
  • 通讯作者: 刘晓军,女,教授,主要从事妇科恶性肿瘤研究,(E-mail)liuxiaojun20211108@163.com。
  • 作者简介:王之丰(1977-),男,安徽芜湖人,主治医师,学士,主要从事妇科恶性肿瘤研究,(E-mail)wangzf415@163.com。
  • 基金资助:
    *本课题受上海市老龄化和妇儿健康研究专项计划任务书(No.2020YJZX0210)和计生专项科研课题(应用新技术筛查女性宫颈,妇科恶性肿瘤的研究)(No.19JSZ07)资助

LncRNAs ABHD11-AS1 Targets miR-133a to Upregulate EGFR Expression and Promote Ovarian Cancer cell Proliferation

WANG Zhi-feng, SUN Hao, HU Dian, et al   

  1. Department of Gynecology and Obstetrics, Second Affiliated Hospital of Naval Medical University, Shanghai 200003
  • Received:2021-11-26 Online:2022-10-20 Published:2022-10-31

摘要: 目的 研究lncRNAs ABHD11-AS1在卵巢癌细胞和输卵管上皮细胞中的表达,探究其对卵巢癌细胞增殖的影响和作用机制。方法 Real-time PCR检测细胞中lncRNAs ABHD11-AS1和miR-133a的表达,双荧光素酶实验明确二者之间的调控作用;用NC siRNA、ABHD11-AS1 siRNA以及NC mimic、miR-133a mimic和NC inhibitor、miR-133a inhibitor分别转染细胞,CCK-8检测细胞增殖;Real-time PCR以及Western Blot实验检测细胞中EGFR的表达。结果 结果表明,lncRNAs ABHD11-AS1在TOV-112D和CaVO3卵巢癌细胞系中的表达水平明显高于TEC细胞,且下调lncRNAs ABHD11-AS1可明显抑制卵巢癌细胞的增殖;ABHD11-AS1与miR-133a的表达呈负相关。双荧光素酶结果显示,转染miR-133a mimic和野生型ABHD11-AS1片段的细胞中荧光素酶的活性显著降低;与输卵管上皮细胞相比,miR-133a在卵巢癌细胞系的表达水平更低。转染miR-133a mimic会显著上调上述两种细胞中miR-133a的表达同时还抑制其增殖和EGFR表达。此外,下调miR-133a可明显促进卵巢癌细胞的增殖以及增加EGFR表达。与此相反,下调lncRNAs ABHD11-AS1明显降低EGFR表达。结论 lncRNAs ABHD11-AS1通过调控miR-133a,上调其下游靶基因EGFR的表达从而促进卵巢癌的发生发展。

关键词: lncRNAs ABHD11-AS1, miR-133a, 卵巢癌, 增殖

Abstract: Objective To investigate the expression of LncRNAs ABHD11-AS1 in ovarian cancer cell and oviductal epithelial cell and explore the effect of LncRNAs ABHD11-AS1 on ovarian cancer cell proliferation. Methods The level of LncRNAs ABHD11-AS1 and miR-133a was detected by Real-time PCR, and interaction between them was confirmed by Dual- Luciferase reporter assay (DR). Cells were transfected with NC siRNA, ABHD11-AS1 as well as siRNA NC mimic, miR-133a mimic and NC inhibitor and miR-133a inhibitor, respectively, and the proliferation was detected by Cell Counting Kit-8 (CCK-8) assay. Real-time PCR and western blotting were performed to detect the EGFR expression. Results Downregulation of lncRNAs ABHD11-AS1 could significantly inhibit the proliferation of ovarian cancer cells. Moreover, lncRNAs ABHD11-AS1 was negatively correlated with the expression of miR-133a. DR results showed that luciferase activity was significantly reduced in cells transfected with miR-133a mimic and wild-type ABHD11-AS1 fragments; and the level of miR-133a was lower in ovarian cancer cell compared to oviductal epithelial cells. Transfection of miR-133a mimic significantly upregulated miR-133a expression in both of these cells and inhibited their proliferation and EGFR expression. In addition, downregulating miR-133a significantly promoted the proliferation of ovarian cancer cells and increased the EGFR expression, while downregulating LncRNAs ABHD11-AS1 significantly decreased the EGFR expression. Conclusion LncRNAs ABHD11-AS1 promoted the malignant behaviors of ovarian cancer by targeting miR-133a to upregulate its downstream target gene EGFR.

Key words: LncRNAsABHD11-AS1, MiR-133a, Ovarian cancer, Proliferation

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