Evidence map›Paper›PMID 29956457›Full record

ArticleJournal of cellular and molecular medicine2018

Lipopolysaccharide enhances ADAR2 which drives Hirschsprung's disease by impairing miR-142-3p biogenesis.

Lei Peng, Hua Zhang, Yang Su, Qiyang Shen, Chunxia Du, Hua Xie, Hongxing Li, Jin Yan, Ziyang Shen, Weiwei Jiang and 3 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. RNA modifications in cancer.British journal of cancer · 2023
    Review
  8. Article
  9. Corrigendum.Journal of cellular and molecular medicine · 2019
    Article
  10. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Lei PengDepartment of Gastroenterology, First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Hua ZhangDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Yang SuDepartment of Hepatobiliary & Pancreatic Surgery, The Affiliated Huaian No.1 Peoples Hospital of Nanjing Medical University, Huaian, China.
Qiyang ShenDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Chunxia DuDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Hua XieDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Hongxing LiDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Jin YanDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Ziyang ShenDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Weiwei JiangDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Yankai XiaMinistry of Education, Key Laboratory of Modern Toxicology, Nanjing Medical University, Nanjing, China.
Xiaoqun XuDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.
Weibing TangDepartment of Pediatric Surgery, Children's Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0002-3582-3408
Ministry of Education · KRSecond Affiliated Hospital of Nanjing Medical University · CNHuaian First People’s Hospital · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Researches over the past decade suggest that lipopolysaccharide is a dominant driver of gastrointestinal motility and could damage the enteric neuron of rat or porcine. However, it remains poorly defined whether LPS participates in Hirschsprung's disease (HSCR). Here, we discovered that LPS increased in HSCR tissues. Furthermore, LPS treatment suppressed the proliferation and differentiation of neural precursor cells (NPCs) or proliferation and migration of human 293T cells. ADAR2 (adenosine deaminase acting on RNA2)-mediated post-transcriptional adenosine-to-inosine RNA editing promotes cancer progression. We show that increased LPS activates ADAR2 and subsequently regulates the A-to-I RNA editing which suppresses the miR-142 expression. RNA sequencing combined with qRT-PCR suggested that ADAR2 restrain cell migration and proliferation via pri-miR-142 editing and STAU1 up-regulation. In conclusion, the findings illustrate that LPS participates in HSCR through the LPS-ADAR2-miR-142-STAU1 axis.

Indexed as

Adenosine DeaminaseAnimalsCell DifferentiationCell MovementCell ProliferationCytoskeletal ProteinsFemaleHEK293 CellsHirschsprung DiseaseHumansInfantIntestinesLipopolysaccharidesMaleMiceMice, Inbred ICRADARB1 protein, humanAdenosine DeaminaseCytoskeletal ProteinsLipopolysaccharidesMicroRNAsMIRN142 microRNA, humanRNA-Binding ProteinsSTAU1 protein, humanA-to-I editingHirschsprung's diseaselipopolysaccharidemigrationproliferation

Identifiers

PMID29956457
PMCPMC6111854
OpenAlexW2810908733

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.