Evidence map›Paper›PMID 30431069›Full record

ArticleInternational journal of oncology2019

Long non-coding RNA HOTAIR mediates the switching of histone H3 lysine 27 acetylation to methylation to promote epithelial-to-mesenchymal transition in gastric cancer.

Yue Song, Rui Wang, Li-Wei Li, Xi Liu, Yun-Fei Wang, Qi-Xue Wang, Qingyu Zhang

Open access · hybridAbstract read
In one paragraph

Article in International journal of oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

73 citing papers in PubMed, 104 citations in OpenAlex.

  1. Review
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  3. Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026
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  17. Effect of tumor exosome-derived Lnc RNA HOTAIR on the growth and metastasis of gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023
    Article
  18. Review
  19. Article
  20. Review

13 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

7 authors at 3 institutions in 1 country.

Yue SongDepartment of Phase I Clinical Trial, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300000, P.R. China.
Rui WangDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Li-Wei LiDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Xi LiuDepartment of Gastroenterology, Tianjin Nankai Hospital, Tianjin 300000, P.R. China.
Yun-Fei WangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Qi-Xue WangDepartment of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Qingyu ZhangDepartment of Gastroenterology, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Tianjin Medical University General Hospital · CNTianjin Medical University Cancer Institute and Hospital · CNTianjin Nankai Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HOX transcript antisense intergenic RNA (HOTAIR), a well‑known long non‑coding RNA, plays an important role in the regulation of epithelial‑to‑mesenchymal transition (EMT). In this study, we propose a novel mechanism through which HOTAIR promotes EMT by switching histone H3 lysine 27 acetylation to methylation at the E‑cadherin promoter, which induces the transcriptional inhibition of E‑cadherin. HOTAIR recruits polycomb repressive complex 2 (PRC2) to catalyze H3K27me3; however, whether HOTAIR is associated with the acetylation of histone H3 lysine 27, a marker of transcriptional activation, and the mechanisms through which HOTAIR triggers the metastasis of gastric cancer (GC) by epigenetic regulation remain largely unknown. In this study, HOTAIR knockdown significantly reversed EMT by increasing the expression of E‑cadherin in GC cells. Additionally, the loss of PRC2 activity induced by HOTAIR knockdown resulted in a global decrease in H3K27 methylation and an increase in H3K27 acetylation. Furthermore, HOTAIR recruits PRC2 (which consists of H3K27 methyltransferase EZH2, SUZ12 and EED), which may inhibit the reaction between the acetyltransferase CBP and H3K27 acetylation. On the whole, the findings of this study suggested that the HOTAIR‑mediated acetylation to methylation switch was associated with the transcriptional inhibition of E‑cadherin. HOTAIR can promote the development of GC through the epigenetic regulation of E‑cadherin, switching the state of the E‑cadherin promoter from the transcriptionally active to the transcriptionally repressive state.

Indexed as

3' Untranslated RegionsAcetylationAnimalsAntigens, CDCadherinsCell Line, TumorEpigenesis, GeneticEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHistonesHumansMethylationMiceNeoplasm TransplantationPromoter Regions, GeneticRNA, Long Noncoding3' Untranslated RegionsAntigens, CDCadherinsCDH1 protein, humanHistonesHOTAIR long untranslated RNA, humanRNA, Long Noncodingepithelial-to-mesenchymal transitiongastric cancerhistone modificationHOTAIRmolecular biomarker

Identifiers

PMID30431069
PMCPMC6254860
OpenAlexW2899848055

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.