文章摘要
高 佳,金慧成,应荣超,刘信春,朱阿考.CCAT1在结直肠癌中海绵吸附miR-210-5p促进肿瘤进展[J].,2020,(12):2224-2228
CCAT1在结直肠癌中海绵吸附miR-210-5p促进肿瘤进展
CCAT1 Promotes Progression in Colorectal Cancer Via Binding miR-210-5p
投稿时间:2020-02-03  修订日期:2020-02-28
DOI:10.13241/j.cnki.pmb.2020.12.005
中文关键词: CCAT1  结直肠癌  miR-210-5p
英文关键词: CCAT1  Colorectal cancer  miR-210-5p
基金项目:浙江省自然科学基金项目(Y18H160291)
作者单位E-mail
高 佳 南京医科大学附属杭州医院 浙江 杭州 310000 1921044512@qq.com 
金慧成 杭州市第一人民医院 浙江 杭州 310000  
应荣超 1 南京医科大学附属杭州医院 浙江 杭州 3100002 杭州市第一人民医院 浙江 杭州 310000  
刘信春 杭州市第一人民医院 浙江 杭州 310000  
朱阿考 杭州市第一人民医院 浙江 杭州 310000  
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中文摘要:
      摘要 目的:探索长链非编码RNA Colon cancer associated transcript-1(CCAT1)在结直肠癌发生发展过程中的作用及可能的分子机制。方法:通过反转录-荧光实时定量PCR(RT-qPCR)检测15对结直肠癌组织和相应的癌旁组织中CCAT1的表达水平;通过RT-qPCR,比较结直肠癌细胞系RKO细胞和正常结肠细胞NCM460中 CCAT1表达量的差异;在结直肠癌细胞系RKO细胞中,我们敲低了CCAT1的表达水平,并用CCK8法和Transwell侵袭实验分别检测了RKO细胞增殖能力和侵袭能力的变化。通过全转录组测序,我们分析了在CCAT1沉默后差异表达的基因,并通过挽救实验和过表达实验进一步验证可能的分子机制。结果:结直肠癌组织和RKO细胞中的CCAT1表达水平均显著高于对应的癌旁组织和NCM460细胞(P<0.001,P<0.005)。结直肠癌细胞系RKO细胞的增殖能力和侵袭能力随着CCAT1水平的降低而显著下降(P<0.005)。全转录组测序结果显示,在CCAT1被沉默后,miR-210-5p的表达量显著升高(P<0.005)。在细胞增殖能力随CCAT1表达水平降低的RKO细胞中转入miR-210-5p inhibitors后,细胞增殖能力显著提高(P<0.05)。相对的,在正常RKO细胞中转入miR-210-5p mimics 以后,细胞增殖能力显著下降(P<0.05)。结论:CCAT1通过海绵吸附miR-210-5p促进结直肠癌的进展,有望成为结直肠癌诊断治疗的新靶点。
英文摘要:
      ABSTRACT Objective: To explore the role of long non-coding RNA Colon cancer associated transcript-1 (CCAT1) in colorectal cancer(CRC)and its possible underlying molecular mechanism. Methods: The expression of CCAT1 in 15 pairs of CRC tissues and corresponding adjacent tissues was detected by reverse transcription-fluorescence real-time quantitative PCR (RT-qPCR). The difference of CCAT1 expression between CRC cell line RKO cells and normal colon cells NCM460 was compared by RT-qPCR. In RKO cells, we knocked down the expression level of CCAT1, and detected the changes of proliferation and invasion ability of RKO cells by CCK8 and transwell invasion assay, respectively. Through full transcriptome sequencing, we analyzed the differentially expressed genes after CCAT1 silencing, and further verified the possible molecular mechanism through a rescue assay and an overexpression assay. Results: the expression level of CCAT1 in CRC tissues and RKO cells was significantly higher than that in corresponding adjacent tissues and NCM460 cells. The proliferation and invasion ability of RKO cells decreased significantly with the decrease of CCAT1 level. The results of full transcriptome sequencing showed that the expression of miR-210-5p increased significantly after CCAT1 was silenced. When miR-210-5p inhibitor were transferred into RKO cells with the decrease of CCAT1 expression level, the cell proliferation ability was significantly improved. In contrast, the ability of cell proliferation decreased significantly after miR-210-5p mimic was transferred into normal RKO cells. Conclusion: CCAT1 promotes the progression of CRC through sponge adsorption of miR-210-5p, and is expected to become a new target for diagnosis and treatment of CRC.
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