Evidence map›Paper›PMID 29219178›Full record

ArticleJournal of cellular physiology2018

The long noncoding RNA NEAT1 contributes to hepatocellular carcinoma development by sponging miR-485 and enhancing the expression of the STAT3.

Xu-Nan Zhang, Jun Zhou, Xiao-Jie Lu

Abstract read
In one paragraph

Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Review
  3. HCC-Related lncRNAs: Roles and Mechanisms.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Review
  6. miRNA in Molecular Diagnostics.Bioengineering (Basel, Switzerland) · 2022
    Review
  7. Review
  8. Recent advances of NEAT1-miRNA interactions in cancer.Acta biochimica et biophysica Sinica · 2022
    Review
  9. Article
  10. Article
  11. Long noncoding RNAJournal of gastrointestinal oncology · 2021
    Article
  12. Article
  13. Article
  14. Long Non-coding RNAs in Cisplatin Resistance in Osteosarcoma.Current treatment options in oncology · 2021
    Review
  15. Review
  16. Genome-wide screening of circadian and non-circadian impact of Neat1 genetic deletion.Computational and structural biotechnology journal · 2021
    Article
  17. Review
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Xu-Nan ZhangDepartment of Imaging, Shanghai Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Jun ZhouDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xiao-Jie LuDepartment of General Surgery, Department of liver Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Jiangsu Province Hospital · CNShanghai East Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Accumulating evidence has supported the significance of lncRNAs in tumorigenesis. Recently, some studies indicate the oncogenic role of lncRNA Nuclear Enriched Abundant Transcript 1 (NEAT1) in hepatocellular carcinoma (HCC). In our present study, we focused on the biological mechanisms through which NEAT1 can regulate HCC development. We found that NEAT1 was greatly upregulated in human HCC cell lines including Huh7, Hep3B, HepG2, Bel-7404, and SK-Hep1 cells compared to the normal human liver cell line LO2. In addition, we observed that miR-485 was significantly downregulated in HCC cells. It was implied that miR-485 was increased by sh-NEAT1 and miR-485 can modulate NEAT1 expression negatively. Meanwhile, NEAT1inhibiton can repress HCC growth, migration, and invasion capacity in HepG2 and Hep3B cells. Through performing bioinformatic analysis, dual-luciferase reporter test, RNA-binding protein immunoprecipitation, and RNA pull-down assay, miR-485 was confirmed as a interacting target of NEAT1. Additionally, STAT3 was recognized as a direct target of miR-485 and miR-485 mimics can inhibit STAT3 expression. It was demonstrated that NEAT1 can increase STAT3 levels while miR-485 mimics can repress STAT3. Moreover, we found that sh-STAT3 was able to restrain HCC cell migration and invasion process. NEAT1 can act as a competing endogenous lncRNA (ceRNA) to regulated STAT3 by sponging miR-485 in HCC. Taken these together, NEAT1 can be used as an important biomarker in HCC diagnosis and treatment.

Indexed as

CarcinogenesisCarcinoma, HepatocellularCell LineCell Line, TumorCell MovementCell ProliferationDown-RegulationGene Expression Regulation, NeoplasticHEK293 CellsHep G2 CellsHumansLiver NeoplasmsMicroRNAsRNA, Long NoncodingSTAT3 Transcription FactorUp-RegulationMicroRNAsMIRN485 microRNA, humanNEAT1 long non-coding RNA, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription Factorhepatocellular carcinomamiR-485NEAT1STAT3

Identifiers

PMID29219178
PMCPMC13482418
OpenAlexW2772737748

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.