A novel circular RNA, circ-ATAD1, contributes to gastric cancer cell progression by targeting miR-140-3p/YY1/PCIF1 signaling axis

被引:28
|
作者
Zhang, Liwei [1 ]
Chang, Xiaohua [2 ]
Zhai, Tingting [3 ]
Yu, Jing [1 ]
Wang, Wenbin [1 ]
Du, Aiping [1 ]
Liu, Na [4 ]
机构
[1] Qiqihar Med Univ, Dept Gastroenterol, Affiliated Hosp 2, Qiqihar 161000, Peoples R China
[2] First Hosp Harbin, Dept Gastroenterol, Harbin 150000, Peoples R China
[3] Qiqihar Med Univ, Dept Operat, Affiliated Hosp 2, Qiqihar 161000, Peoples R China
[4] Qiqihar Med Univ, Dept Hematopathol, Affiliated Hosp 2, Qiqihar 161000, Peoples R China
关键词
Gastric cancer; Circular RNA; Circ-ATAD1; miR-140-3p; YY1; PCIF1; GROWTH; MIGRATION;
D O I
10.1016/j.bbrc.2020.02.100
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Circular RNAs (circRNAs) has been shown to be involved in the progression of various malignancies. Nevertheless, the mechanism of dysregulated circRNAs in gastric cancer (GC) remains to be understood. CircRNA microarray was utilized for identifying circRNA expression profiles in GC tissues. Circ-ATAD1 expression was measured by qRT-PCR. The clinical significance of circ-ATAD1 was analyzed by Fisher's exact test, Kaplan-Meier plots, and Cox regression model. The function of circ-ATAD1 was explored by using CCK-8, clone formation, flow cytometric and transwell experiments. RNA sequencing, bioinformatics, RNA pulldown, chromatin immunoprecipitation followed by sequencing, and dual-luciferase reporter assays were applied to determine the regulatory networks of circ-ATAD1 in GC cells. CircATAD1 expression was increased in cancerous tissues. The prognostic value of circ-ATAD1 was identified in GC patients. For GC cells, circ-ATAD1 increased cell progression by sponging miR-140-3p to upregulate YY1. Additionally, YY1 directly bound to the promoter of PCIF1, thereby activating its transcription. Collectively, circ-ATAD1 plays an important role in GC tumorigenesis and progression and might be an important biomarker/therapeutic target for GC. (C) 2020 Elsevier Inc. All rights reserved.
引用
收藏
页码:841 / 849
页数:9
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