文章摘要
赵刚,武青生,赵延礼,等.长链非编码 RNA NR2F1-AS1靶向微小 RNA-145-5p调控结肠癌细胞增殖、迁移和侵袭的分子机制[J].安徽医药,2022,26(2):373-377.
长链非编码 RNA NR2F1-AS1靶向微小 RNA-145-5p调控结肠癌细胞增殖、迁移和侵袭的分子机制
Molecular mechanism of lnc RNA NR2F1-AS1 targeting miR-145-5p to regulate colon cancer cell proliferation, migration and invasion
  
DOI:10.3969/j.issn.1009-6469.2022.02.039
中文关键词: 结肠肿瘤  核受体亚家族 2,F组,成员 1  NR2F1-AS1  微小 RNA-145-5p  增殖  迁移  侵袭
英文关键词: Colonic neoplasms  Nuclear receptor subfamily 2,group F,member 1  NR2F1-AS1  MiR-145-5p  Proliferation  Migration  Invasion
基金项目:
作者单位
赵刚 青海省第五人民医院普通外科青海西宁 810000 
武青生 青海省第五人民医院普通外科青海西宁 810000 
赵延礼 青海大学医学院生理学教研室青海西宁 810000 
马生彪 青海省第五人民医院普通外科青海西宁 810000 
王巍 青海省第五人民医院普通外科青海西宁 810000 
穆元忠 青海省第五人民医院普通外科青海西宁 810000 
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中文摘要:
      目的探讨长链非编码 RNA(lnc RNA)核受体亚族 2F组成员 1反义 RNA(NR2F1-AS1)对结肠癌细胞增殖、迁移和侵袭的影响及作用机制。方法收集 2015年 3月至 2017年 5月青海省第五人民医院外科手术切除并经病理证实为原发性结肠腺癌组织 25例,另留取距肿瘤边缘 3 cm的癌旁组织(正常结肠组织)。实时荧光定量 PCR(RT-qPCR)检测结肠癌组织和癌旁组织中 NR2F1-AS1和微小 RNA-145-5p(miR-145-5p)表达水平。以结肠癌细胞 HCT116为研究对象,双荧光素酶报告基因实验验证 NR2F1-AS1和 miR-145-5p调控关系。转染 NR2F1-AS1小干扰 RNA或 miR-145-5p模拟物至 HCT116细胞,细胞计数试剂盒( CCK-8)和 Transwell分别检测干扰 NR2F1-AS1表达或过表达 miR-145-5p对 HCT116细胞增殖、迁移和侵袭的影响。结果与癌旁组织比较,结肠癌组织中 NR2F1-AS1表达升高[( 3.39±0.33)比( 1.01±0.11)P<0.05]miR-145-5p表达降低[( 0.55±
英文摘要:
      Objective To investigate the effect and mechanism of lnc RNA NR2F1-AS1 on the proliferation, migration and invasion of colon cancer cells.Methods From March 2015 to May 2017, 25 patients with primary colorectal adenocarcinoma confirmed by pa.thology and surgically resected in The Fifth People's Hospital of Qinghai Province were collected. Paracancental tissue (normal colontissue) 3 cm away from the tumor edge was also collected. The expression levels of NR2F1-AS1 and miR-145-5p in colon cancer tissues and adjacent tissues were detected by RT-qPCR. The colon cancer cell HCT116 was used as the research object, and the double lucifer.ase reporter gene experiment verified the regulatory relationship between NR2F1-AS1 and miR-145-5p. NR2F1-AS1 small interfering RNA or miR-145-5p mimic was transfected into HCT116 cells. CCK-8 and Transwell were used to detect the effect of interfering with NR2F1-AS1 expression or over-expressing miR-145-5p on the proliferation, migration and invasion of HCT116 cells.Results Com. pared with adjacent tissues, the expression of NR2F1-AS1 in colon cancer tissues increased [(3.39±0.33) vs. (1.01±0.11), P<0.05], and the expression of miR-145-5p decreased[(0.55±0.05) vs. (1.00±0.08), P<0.05]. Compared with the miR-NC group co-transfected with WT-NR2F1-AS1, the luciferase activity in miR-145-5p group was reduced (P<0.05). After over-expressing NR2F1-AS1, the expression level of miR-145-5p in cells decreased (P<0.05), and the expression level of miR-145-5p in cells increased after interfering with sNR2F1-AS1 expression (P<0.05). After interfering with sNR2F1-AS1 expression or over-expressing miR-145-5p, the OD value, HCT116 cells migration and invasion numbers were decreased (P<0.05). Interfering with miR-145-5p expression reversed the effect of interfering with NR2F1-AS1 expression on HCT116 cells OD value, migration and invasion numbers.Conclusion NR2F1-AS1 is highly expressed in colon cancer tissues. Interfering with NR2F1-AS1 expression may inhibit colon cancer cell proliferation, migration and invasion by up-regulating miR-145-5p expression, and is a potential target for colon cancer treatment.
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