Evidence map›Paper›PMID 32945505›Full record

ArticleMolecular medicine reports2020

Long non‑coding RNA NEAT1 modifies cell proliferation, colony formation, apoptosis, migration and invasion via the miR‑4500/BZW1 axis in ovarian cancer.

Hongying Xu, Xiaowei Sun, Ying Huang, Qin Si, Maokun Li

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 25 citations in OpenAlex.

  1. Molecular Insights into BZW1 Expression and [Molecular imaging and biology · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. The Role of Long Non-Coding RNAs in Ovarian Cancer Cells.International journal of molecular sciences · 2024
    Review
  6. Emerging roles of the long non-coding RNA NEAT1 in gynecologic cancers.Journal of cell communication and signaling · 2023
    Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Recent advances of NEAT1-miRNA interactions in cancer.Acta biochimica et biophysica Sinica · 2022
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  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

5 authors at 1 institution in 1 country.

Hongying XuDepartment of Gynecology, Jingzhou Hospital of Traditional Chinese Medicine, The Third Clinical Medical College of Yangtze University, Jingzhou, Hubei 434000, P.R. China.
Xiaowei SunDepartment of Internal Medicine, Jingzhou Hospital of Traditional Chinese Medicine, The Third Clinical Medical College of Yangtze University, Jingzhou, Hubei 434000, P.R. China.
Ying HuangDepartment of Gynecology, Jingzhou Hospital of Traditional Chinese Medicine, The Third Clinical Medical College of Yangtze University, Jingzhou, Hubei 434000, P.R. China.
Qin SiDepartment of Nursing, Jingzhou Hospital of Traditional Chinese Medicine, The Third Clinical Medical College of Yangtze University, Jingzhou, Hubei 434000, P.R. China.
Maokun LiDepartment of Surgery, Jingzhou Hospital of Traditional Chinese Medicine, The Third Clinical Medical College of Yangtze University, Jingzhou, Hubei 434000, P.R. China.
Yangtze University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ovarian cancer (OC) is a frequently occurring malignant tumor in women. Increasing evidence has indicated that long non‑coding RNA (lncRNA) nuclear paraspeckle assembly transcript 1 (NEAT1) participates in OC pathogenesis. Thus, the aim of the present study was to explore the function of NEAT1 during OC progression. The expression levels of NEAT1, microRNA (miR)‑4500 and basic leucine zipper and W2 domain‑containing protein 1 (BZW1) were assessed via reverse transcription‑quantitative PCR and western blotting. Furthermore, cell proliferation, colony formation, apoptosis, migration and invasion were assessed using Cell‑Counting Kit 8, colony formation, flow cytometry and Transwell assays, respectively. Cell glycolysis was analyzed using an XF96 metabolic flux analyzer, and the relationship between miR‑4500 and NEAT1 or BZW1 was verified via dual‑luciferase reporter and RNA binding protein immunoprecipitation assays. miR‑4500 expression levels were low, whereas NEAT1 expression levels were high in OC tissues and cell lines compared with control tissues and cell lines. Moreover, the results indicated that NEAT1 was a sponge of miR‑4500, which directly targeted BZW1. NEAT1 knockdown induced OC cell apoptosis, and inhibited OC cell proliferation, colony formation, migration, invasion and glycolysis. miR‑4500 inhibitor reversed NEAT1 knockdown‑mediated effects. Similarly, miR‑4500 mimic‑mediated effects on cell functions were reversed by BZW1 overexpression. In addition, the results indicated that BZW1 expression was regulated by NEAT1 and miR‑4500. Collectively, the present study suggested that NEAT1 modulated cell proliferation, colony formation, apoptosis, migration, invasion and glycolysis via the miR‑4500/BZW1 axis in OC; therefore, NEAT1 may serve as a therapeutic target for OC.

Indexed as

ApoptosisCase-Control StudiesCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationDisease ProgressionDNA-Binding ProteinsFemaleGene Expression Regulation, NeoplasticGlycolysisHumansMicroRNAsOvarian NeoplasmsRNA, Long NoncodingBZW1 protein, humanCell Cycle ProteinsDNA-Binding ProteinsmicroRNA 4500, humanMicroRNAsNEAT1 long non-coding RNA, humanRNA, Long Noncoding

Identifiers

PMID32945505
PMCPMC7453653
OpenAlexW3047365337

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.