Evidence map›Paper›PMID 27659532›Full record

ArticleOncotarget2016

Promoter methylation of PCDH10 by HOTAIR regulates the progression of gastrointestinal stromal tumors.

Na Keum Lee, Jung Hwa Lee, Won Kyu Kim, Seongju Yun, Young Hoon Youn, Chan Hyuk Park, Yun Young Choi, Hogeun Kim, Sang Kil Lee

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.

  1. Pooled it
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  14. The Nefarious Nexus of Noncoding RNAs in Cancer.International journal of molecular sciences · 2018
    Review
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  16. Review
  17. Article
  18. Molecular characterization and pathogenesis of gastrointestinal stromal tumor.Translational gastroenterology and hepatology · 2018
    Review
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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

9 authors at 1 institution in 1 country.

Na Keum LeeYonsei Institute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Jung Hwa LeeYonsei Institute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Won Kyu KimDepartment of Pathology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Seongju YunDepartment of Pathology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Young Hoon YounYonsei Institute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Chan Hyuk ParkYonsei Institute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Yun Young ChoiYonsei Institute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Hogeun KimDepartment of Pathology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Sang Kil LeeYonsei Institute of Gastroenterology, Department of Internal Medicine, Yonsei University College of Medicine, South Korea.
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HOTAIR, a long non-coding RNA (lncRNA), plays a crucial role in tumor initiation and metastasis by interacting with the PRC2 complex and the modulation of its target genes. The role of HOTAIR in gastrointestinal stromal tumors (GISTs) is remains unclear. Herein we investigate the mechanism of HOTAIR in the genesis and promotion of GISTs. The expression of HOTAIR was found to be higher in surgically resected high-risk GISTs than that in low- and intermediate-risk GISTs. Using GIST-T1 and GIST882 cells, we demonstrated that HOTAIR repressed apoptosis, was associated with cell cycle progression, and controlled the invasion and migration of GIST cells. Using a gene expression microarray and lists of HOTAIR-associated candidate genes, we suggested that protocadherin 10 (PCDH10) is a key molecule. PCDH10 expression was significantly decreased in GIST-T1 and GIST882 cells, possibly as a consequence of hypermethylation. We observed that HOTAIR induced PCDH10 methylation in a SUZ12-dependent manner. In this study, we found that the malignant character of GISTs was initiated and amplified by PCDH10 in a process regulated by HOTAIR. In summary, our findings imply that PCDH10 and HOTAIR may be useful markers of disease progression and therapeutic targets.

Indexed as

DNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticPromoter Regions, GeneticApoptosisAzacitidineCadherinsCell Cycle CheckpointsCell Line, TumorCell ProliferationDisease ProgressionGastrointestinal Stromal TumorsGene SilencingHumansProtocadherinsRNA, Long NoncodingAzacitidineCadherinsHOTAIR long untranslated RNA, humanPCDH10 protein, humanProtocadherinsRNA, Long Noncodinggastrointestinal stromal tumorHOTAIRPCDH10

Identifiers

PMID27659532
PMCPMC5342742
OpenAlexW2523091798

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.