Literature DB >> 33449226

Circ_0004104 Accelerates the Progression of Gastric Cancer by Regulating the miR-539-3p/RNF2 Axis.

Furong Yue1, Keyu Peng1, Li Zhang1, Jun Zhang2.   

Abstract

BACKGROUND: Circular RNA (circRNA) has been shown to be closely associated with cancer progression, including gastric cancer (GC). However, the function of circ_0004104 in GC progression has not been clarified. AIMS: The purpose of this study was to explore the role of circ_0004104 in GC progression.
METHODS: The expression levels of circ_0004104, miR-539-3p, and ring finger protein 2 (RNF2) were assessed using quantitative real-time polymerase chain reaction. Cell proliferation was measured by 3-(4,5-dimethyl-2 thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, and cell migration and invasion were detected using transwell assay. The levels of glutamine, glutamate, and α-ketoglutarate were determined to evaluate the glutaminolysis of cells, and the protein levels of glutaminolysis-related markers and RNF2 were detected using western blot analysis. Furthermore, Dual-Luciferase Reporter Assay was employed to assess the interaction between miR-539-3p and circ_0004104 or RNF2. Animal experiments were carried out to evaluate the effect of circ_0004104 silencing on GC tumor growth in vivo.
RESULTS: Circ_0004104 was upregulated in GC, and its knockdown repressed the proliferation, metastasis, and glutaminolysis of GC cells in vitro and reduced GC tumor growth in vivo. Furthermore, we discovered that circ_0004104 could sponge miR-539-3p and miR-539-3p could target RNF2. The rescue experiments suggested that miR-539-3p inhibitor could reverse the suppressive effect of circ_0004104 silencing on GC progression, and RNF2 overexpression also reversed the inhibition effect of miR-539-3p mimic on GC progression.
CONCLUSION: Circ_0004104 accelerated GC progression via regulating the miR-539-3p/RNF2 axis, indicating that circ_0004104 might be a potential therapeutic target for GC.
© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.

Entities:  

Keywords:  Circ_0004104; Gastric cancer; RNF2; miR-539-3p

Mesh:

Substances:

Year:  2021        PMID: 33449226     DOI: 10.1007/s10620-020-06802-5

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  3 in total

1.  miR-539-3P inhibits proliferation and invasion of gastric cancer cells by targeting CTBP1.

Authors:  Jia Zhou; Mingqi Su; Hui Zhang; Jialiang Wang; Ying Chen
Journal:  Int J Clin Exp Pathol       Date:  2019-05-01

Review 2.  Pathogenesis of Gastric Cancer: Genetics and Molecular Classification.

Authors:  Ceu Figueiredo; M C Camargo; Marina Leite; Ezequiel M Fuentes-Pananá; Charles S Rabkin; José C Machado
Journal:  Curr Top Microbiol Immunol       Date:  2017       Impact factor: 4.291

3.  MicroRNA‑539 inhibits the proliferation and migration of gastric cancer cells by targeting SRY‑box 5 gene.

Authors:  Shi Ding; Yanping Zhang
Journal:  Mol Med Rep       Date:  2019-07-11       Impact factor: 2.952

  3 in total
  5 in total

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Journal:  Cell Cycle       Date:  2022-02-28       Impact factor: 5.173

Review 2.  Circular RNAs Involve in Immunity of Digestive Cancers From Bench to Bedside: A Review.

Authors:  Chunyue Chen; Congcong Xia; Hao Tang; Yirun Jiang; Shan Wang; Xin Zhang; Tao Huang; Xiaoqing Yuan; Junpu Wang; Li Peng
Journal:  Front Immunol       Date:  2022-04-04       Impact factor: 8.786

3.  Circ_0000620 acts as an oncogenic factor in gastric cancer through regulating MMP2 expression via sponging miR-671-5p.

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Journal:  J Biol Res (Thessalon)       Date:  2021-12-31       Impact factor: 1.889

4.  MiR-539-3p inhibited chondrogenic differentiation in human adipose stem cells by targeting Sox9.

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Journal:  J Orthop Surg Res       Date:  2022-03-18       Impact factor: 2.359

Review 5.  Gastric cancer: An epigenetic view.

Authors:  Si-Yuan Tang; Pei-Jun Zhou; Yu Meng; Fu-Rong Zeng; Guang-Tong Deng
Journal:  World J Gastrointest Oncol       Date:  2022-01-15
  5 in total

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