Evidence map›Paper›PMID 31481527›Full record

ArticleBioscience reports2019

Long non-coding RNA-NEAT1, a sponge for miR-98-5p, promotes expression of oncogene HMGA2 in prostate cancer.

Zhuifeng Guo, Chang He, Fan Yang, Liang Qin, Xuwei Lu, Jiawen Wu

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Recent advances of NEAT1-miRNA interactions in cancer.Acta biochimica et biophysica Sinica · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. 3' UTR-truncated HMGA2 overexpression induces non-malignantMolecular therapy. Methods & clinical development · 2021
    Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Association ofPharmacogenomics and personalized medicine · 2021
    Article
  16. Review
  17. Article
  18. Article
  19. Observational
  20. Article
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

6 authors at 1 institution in 1 country.

Zhuifeng GuoDepartment of Urology, Shanghai Minhang Hospital, Fudan University, Shanghai 201199, People's Republic of China.
Chang HeDepartment of Urology, Shanghai Minhang Hospital, Fudan University, Shanghai 201199, People's Republic of China.
Fan YangDepartment of Urology, Shanghai Minhang Hospital, Fudan University, Shanghai 201199, People's Republic of China.
Liang QinDepartment of Urology, Shanghai Minhang Hospital, Fudan University, Shanghai 201199, People's Republic of China.
Xuwei LuDepartment of Urology, Shanghai Minhang Hospital, Fudan University, Shanghai 201199, People's Republic of China.
Jiawen WuDepartment of Urology, Shanghai Minhang Hospital, Fudan University, Shanghai 201199, People's Republic of China hcdoctor@hotmail.com.ORCID 0000-0002-7046-616X
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence demonstrated that noncoding RNAs (lncRNA, miRNA) play important roles in the cancer development. LncRNA NEAT1 functions as an oncogene in many cancers. However, the roles of NEAT1 in prostate cancer (PCa) remain largely unknown. In the present study, we aim to explore the molecular mechanism of NEAT1 in the development of PCa. We detected the expression levels of NEAT1 in a total of 16 benign prostatic hyperplasia tissues (BPH), 30 matched adjacent healthy control (HC) tissues and 30 PCa tissues, as well as PCa cell lines PC-3, DU-145, LNCaP and normal prostate epithelial cell line RWPE-1. The results showed that NEAT1 was significantly up-regulated in PCa tissues and PCa cell lines. Knockdown of NEAT1 can largely inhibit DU-145 and PC-3 cell growth and invasion. Bioinformatics analysis predicted NEAT1 has the binding site of miR-98-5p which can bind to the 3'UTR of HMGA2. And the expression level of NEAT1 has a positive correlation with HMAG2, while negative correlation with miR-98-5p in PCa cells. In addition, luciference assay and RNA immunoprecipitation (RIP) assay confirmed that NEAT1 can function as a competing endogenous RNA (ceRNA) by sponging miR-98-5p to active HMGA2. Moreover, silencing of HMGA2 can decrease the proliferation ability of PCa cells. Taken together, NEAT1/miR-98-5p/HMGA2 pathway is involved in the development and progression of PCa. NEAT1 could be recommended as a prognostic biomarker and inhibition of NEAT1 expression may be a promising strategy for PCa therapy.

Indexed as

AgedBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHMGA2 ProteinHumansMaleMicroRNAsNeoplasm StagingPrognosisProstatic HyperplasiaProstatic NeoplasmsRNA, Long NoncodingUp-RegulationBiomarkers, TumorHMGA2 ProteinHMGA2 protein, humanMicroRNAsMIRN98 microRNA, humanNEAT1 long non-coding RNA, humanRNA, Long NoncodingHMGA2lncRNA NEAT1miR-98-5pprostate cancer

Identifiers

PMID31481527
PMCPMC6757183
OpenAlexW2972199471

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.