Evidence map›Paper›PMID 33299646›Full record

ArticleCancer biology & medicine2020

Coordinated silencing of the Sp1-mediated long noncoding RNA MEG3 by EZH2 and HDAC3 as a prognostic factor in pancreatic ductal adenocarcinoma.

Ting Han, Meng Zhuo, Cuncun Yuan, Xiuying Xiao, Jiujie Cui, Guangrong Qin, Liwei Wang, Feng Jiao

Open access · goldAbstract read
In one paragraph

Article in Cancer biology & medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Advanced biomedical research · 2025
    Review
  3. Article
  4. Article
  5. Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Observational
  13. A Cancer Cell Cluster Marked by LincRNAFrontiers in oncology · 2021
    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

8 authors at 4 institutions in 1 country.

Ting HanDepartment of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China.
Meng ZhuoDepartment of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China.
Cuncun YuanDepartment of Pathology, Fudan University Eye Ear Nose and Throat Hospital, Shanghai 201114, China.
Xiuying XiaoDepartment of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China.
Jiujie CuiDepartment of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China.
Guangrong QinShanghai Center for Bioinformation Technology, Shanghai 201203, China.
Liwei WangDepartment of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China.ORCID 0000-0001-5972-938X
Feng JiaoDepartment of Oncology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200127, China.ORCID 0000-0002-0031-4363
Renji Hospital · CNFudan University · CNShanghai Cancer Institute · CNShanghai Center For Bioinformation Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Pancreatic ductal adenocarcinoma (PDAC) is a disease with high mortality. Many so-called "junk" noncoding RNAs need to be discovered in PDAC. The purpose of this study was therefore to investigate the function and regulatory mechanism of the long noncoding RNA MEG3 in PDAC. Methods: The Gene Expression Omnibus database (GEO database) was used to determine the differential expression of long noncoding RNAs in PDAC, and MEG3 was selected for subsequent verification. Tissue and cell samples were used to verify MEG3 expression, followed by functional detection Results: We generated a catalogue of PDAC-associated long noncoding RNAs in the GEO database. The ectopic expression of MEG3 inhibited PDAC growth and metastasis Conclusions: Reduced MEG3 levels played a crucial role in the PDAC malignant phenotype, which provided insight into novel and effective molecular targets of MEG3 for pancreatic cancer treatment.

Indexed as

AnimalsCarcinoma, Pancreatic DuctalCell ProliferationDown-RegulationEnhancer of Zeste Homolog 2 ProteinFemaleGene Expression Regulation, NeoplasticHistone Deacetylase 3Histone DeacetylasesHumansMaleMice, Inbred BALB CMice, NudeMiddle AgedPancreatic NeoplasmsPrognosisEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHistone Deacetylase 3Histone DeacetylasesMEG3 non-coding RNA, humanRNA, Long NoncodingEZH2HDAC3MEG3miR-374a-5pPancreatic ductal adenocarcinomaSp1

Identifiers

PMID33299646
PMCPMC7721101
OpenAlexW3109705622

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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.