CircNFIX promotes progression of pituitary adenoma via CCNB1 by sponging miR-34a-5p

被引:19
|
作者
Cheng, Jianhua [1 ]
Nie, Ding [1 ]
Li, Bin [2 ]
Gui, SongBai [1 ]
Li, ChuZhong [2 ]
Zhang, YaZhuo [2 ]
Zhao, Peng [1 ]
机构
[1] Capital Med Univ, Neurosurg Dept, Beijing Tiantan Hosp, 119 South Fourth Ring West Rd, Beijing 100070, Peoples R China
[2] Beijing Neurosurg Inst, Dept Cell & Biol, Beijing 100070, Peoples R China
关键词
CircNFIX; MiR-34a-5p; CCNB1; Progression; Pituitary adenoma; CIRCULAR RNAS; CELL-CYCLE; PROLIFERATION; CANCER; ROLES; OVEREXPRESSION; GROWTH; GLIOMA;
D O I
10.1016/j.mce.2020.111140
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Previous studies have shown that CCNB1 affects the invasiveness of pituitary adenomas, and it is of great significance to find the upstream mechanism of regulating CCNB1. In this study, we explored a significantly overexpressed circRNA in invasive pituitary adenomas. Based on bioinformatics analysis and mechanism experiments, we determined that circNFIX (has-circ_0005660) affects cell invasion, migration and proliferation in pituitary adenomas by sponging miR-34a-5p through CCNB1. In pituitary adenoma tissues, the expression of circNFIX and CCNB1 was upregulated, while miR-34a-5p expression was downregulated. The silencing of circNFIX or overexpression of miR-34a-5p inhibited cell invasion, migration and proliferation. Inhibition of miR34a-5p expression reversed the inhibitory effect of circNFIX silencing on the progression of pituitary adenoma. In conclusion, CircNFIX affects cell invasion, migration, and proliferation in pituitary adenomas by sponging miR-34a-5p through CCNB1. Therefore, circNFIX is expected to serve as a potential target for the treatment of pituitary adenomas.
引用
收藏
页数:9
相关论文
共 50 条
  • [21] circPUM1 Promotes Tumorigenesis and Progression of Ovarian Cancer by Sponging miR-615-5p and miR-6753-5p
    Guan, Xue
    Zong, Zhi-hong
    Liu, Yao
    Chen, Shuo
    Wang, Li-li
    Zhao, Yang
    MOLECULAR THERAPY-NUCLEIC ACIDS, 2019, 18 : 882 - 892
  • [22] RP11-295G20.2 facilitates hepatocellular carcinoma progression via the miR-6884-3p/CCNB1 pathway
    Li, Jing
    Xia, Tingting
    Cao, Junyan
    He, Donghong
    Chen, Zhaocong
    Liang, Biao
    Song, Jie
    AGING-US, 2020, 12 (14): : 14918 - 14932
  • [23] LncRNA SNHG7 promotes cardiac remodeling by upregulating ROCK1 via sponging miR-34-5p
    Wang, Jie
    Zhang, Shouwen
    Li, Xinhua
    Gong, Maolei
    AGING-US, 2020, 12 (11): : 10441 - 10456
  • [24] Exosomes regulate doxorubicin resistance in breast cancer via miR-34a-5p/ NOTCH1
    Chen, Nan-nan
    Zhou, Ke-fan
    Miao, Zhuang
    Chen, Yun-xia
    Cui, Jing-xia
    Su, Su -wen
    MOLECULAR AND CELLULAR PROBES, 2024, 76
  • [25] MiR-34a-5p inhibits fibroblast-like synoviocytes proliferation via XBP1
    Song, A-F
    Kang, L.
    Wang, Y-F
    Wang, M.
    EUROPEAN REVIEW FOR MEDICAL AND PHARMACOLOGICAL SCIENCES, 2020, 24 (22) : 11675 - 11682
  • [26] Long non-coding RNA TUG1 promotes endometrial cancer development via inhibiting miR-299 and miR-34a-5p
    Liu, Lifen
    Chen, Xin
    Zhang, Ying
    Hu, Yanrong
    Shen, Xiaoqing
    Zhu, Weipei
    ONCOTARGET, 2017, 8 (19) : 31386 - 31394
  • [27] HCG18/miR-34a-5p/HMMR axis accelerates the progression of lung adenocarcinoma
    Li, Wei
    Pan, Tinghong
    Jiang, Wei
    Zhao, Hongying
    BIOMEDICINE & PHARMACOTHERAPY, 2020, 129
  • [28] Mouse-specific up-regulation of Ccnb1 expression by miR-199a-5p in keratinocyte
    Kim, Bong-Kyu
    Kim, Injung
    Lee, Ah-Reum
    Yoo, Hye-In
    Yoon, Sungjoo Kim
    FEBS OPEN BIO, 2016, 6 (11): : 1131 - 1140
  • [29] LINC00665 functions as a competitive endogenous RNA to regulate AGTR1 expression by sponging miR-34a-5p in glioma
    Dai, Yongyue
    Zhang, Yucheng
    Hao, Maolin
    Zhu, Renwu
    ONCOLOGY REPORTS, 2021, 45 (03) : 1202 - 1212
  • [30] The Long Noncoding RNA NEAT1 Targets miR-34a-5p and Drives Nasopharyngeal Carcinoma Progression via Wnt/β-Catenin Signaling
    Ji, Yuqing
    Wang, Man
    Li, Xueshen
    Cui, Fusheng
    YONSEI MEDICAL JOURNAL, 2019, 60 (04) : 336 - 345