Evidence map›Paper›PMID 24000294›Full record

ArticleGut2014

Long non-coding RNA HNF1A-AS1 regulates proliferation and migration in oesophageal adenocarcinoma cells.

Xue Yang, Jee Hoon Song, Yulan Cheng, Wenjing Wu, Tushar Bhagat, Yiting Yu, John M Abraham, Sariat Ibrahim, William Ravich, Bani Chander Roland and 7 more

Abstract read
In one paragraph

Article in Gut, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 3% 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

135 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Roles of long non-coding RNAs in oesophageal cancer pathogenesis.International journal of experimental pathology · 2025
    Review
  5. [Ferroptosis-related long non-coding RNA to predict the clinical outcome of non-small cell lung cancer after radiotherapy].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2025
    Article
  6. Review
  7. Article
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  10. Article
  11. Review
  12. Article
  13. Article
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  15. Article
  16. mCells · 2022
    Article
  17. Article
  18. Article
  19. Article
  20. Article

75 more citing papers are in PubMed but not listed here.

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

17 authors at 2 institutions in 2 countries.

Xue YangDivision of Gastroenterology, Department of Medicine, Johns Hopkins University School of Medicine, , Baltimore, Maryland, USA.
Jee Hoon Song
Yulan Cheng
Wenjing Wu
Tushar Bhagat
Yiting Yu
John M Abraham
Sariat Ibrahim
William Ravich
Bani Chander Roland
Mouen Khashab
Vikesh K Singh
Eun Ji Shin
Xiao Yang
Amit K Verma
Stephen J Meltzer
Yuriko Mori
Johns Hopkins University · USAlbert Einstein College of Medicine · US

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI Rosalie Wollett · 1985 to 2026
$208.6M
The temporal epigenomic program of Barrett's neoplastic progressionR01DK087454 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI MELTZER, STEPHEN J · 2009 to 2013
$1.8M
The Role of microRNA Alterations in Barrett's CarcinogenesisR01CA146799 · NCI · JOHNS HOPKINS UNIVERSITY · PI MELTZER, STEPHEN J · 2009 to 2012
$1.3M
NCI NIH HHS P30 CA006973NCI NIH HHS R01 CA146799NCI NIH HHS R01CA146799NIDDK NIH HHS R01 DK087454NIDDK NIH HHS R01DK087454
6 · The paper itself

Abstract

objectivesLong non-coding RNAs (lncRNA) have been shown to play important roles in the development and progression of cancer. However, functional lncRNAs and their downstream mechanisms are largely unknown in the molecular pathogenesis of oesophageal adenocarcinoma (EAC) and its progression.

designlncRNAs that are abnormally upregulated in EACs were identified by RNA-sequencing analysis, followed by quantitative RT-PCR (qRTPCR) validation using tissues from 25 EAC patients. Cell biological assays in combination with small interfering RNA-mediated knockdown were performed in order to probe the functional relevance of these lncRNAs.

resultsWe discovered that a lncRNA, HNF1A-AS1, is markedly upregulated in human primary EACs relative to their corresponding normal oesophageal tissues (mean fold change 10.6, p<0.01). We further discovered that HNF1A-AS1 knockdown significantly inhibited cell proliferation and anchorage-independent growth, suppressed S-phase entry, and inhibited cell migration and invasion in multiple in vitro EAC models (p<0.05). A gene ontological analysis revealed that HNF1A-AS1 knockdown preferentially affected genes that are linked to assembly of chromatin and the nucleosome, a mechanism essential to cell cycle progression. The well known cancer-related lncRNA, H19, was the gene most markedly inhibited by HNF1A-AS1 knockdown. Consistent to this finding, there was a significant positive correlation between HNF1A-AS1 and H19 expression in primary EACs (p<0.01).

conclusionsWe have discovered abnormal upregulation of a lncRNA, HNF1A-AS1, in human EAC. Our findings suggest that dysregulation of HNF1A-AS1 participates in oesophageal tumorigenesis, and that this participation may be mediated, at least in part, by modulation of chromatin and nucleosome assembly as well as by H19 induction.

Indexed as

Gene ExpressionAdenocarcinomaCell Line, TumorCell MovementCell ProliferationEsophageal NeoplasmsGene Knockdown TechniquesHumansRNA, Long NoncodingRNA, Small InterferingS Phase Cell Cycle CheckpointsUp-RegulationH19 long non-coding RNARNA, Long NoncodingRNA, Small InterferingCancer GeneticsGene ExpressionOesophageal Cancer

Identifiers

PMID24000294
PMCPMC4612639
OpenAlexW2128876691

What OpenQuestion holds

Textmetadata
LicenceTDM
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.