Evidence map›Paper›PMID 28131418›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2017

The Pseudogene DUXAP8 Promotes Non-small-cell Lung Cancer Cell Proliferation and Invasion by Epigenetically Silencing EGR1 and RHOB.

Ming Sun, Feng-Qi Nie, Chongshuang Zang, Yunfei Wang, Jiakai Hou, Chenchen Wei, Wei Li, Xiang He, Kai-Hua Lu

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
5.5field-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

80 citing papers in PubMed, 125 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Ming SunDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China; Department of Bioinformatics and Computational Biology, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
Feng-Qi NieDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
Chongshuang ZangDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
Yunfei WangDepartment of Bioinformatics and Computational Biology, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
Jiakai HouDepartment of Bioinformatics and Computational Biology, UT MD Anderson Cancer Center, Houston, TX 77030, USA.
Chenchen WeiDepartment of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
Wei LiDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
Xiang HeDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China.
Kai-Hua LuDepartment of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, China. Electronic address: lukaihua110@126.com.
Nanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CNThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, the non-protein-coding functional elements in the human genome have been identified as key regulators in postgenomic biology, and a large number of pseudogenes as well as long non-coding RNAs (lncRNAs) have been found to be transcribed in multiple human cancers. However, only a small proportion of these pseudogenes has been functionally characterized. In this study, we screened for pseudogenes associated with human non-small-cell lung cancer (NSCLC) by comparative analysis of several independent datasets from the GEO. We identified a transcribed pseudogene named DUXAP8 that is upregulated in tumor tissues. Patients with higher DUXAP8 expression exhibited shorter survival, suggesting DUXAP8 as a new candidate prognostic marker for NSCLC patients. Knockdown of DUXAP8 impairs cell growth, migration, and invasion, and induces apoptosis both in vitro and in vivo. Mechanistically, DUXAP8 represses the tumor suppressors EGR1 and RHOB by recruiting histone demethylase LSD1 and histone methyltransferase EZH2, thereby promoting cell proliferation, migration, and invasion. These findings indicate that the pseudogene DUXAP8 may act as an oncogene in NSCLC by silencing EGR1 and RHOB transcription by binding with EZH2 and LSD1, which may offer a novel therapeutic target for this disease.

Indexed as

Epigenesis, GeneticGene SilencingApoptosisCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell ProliferationCell Transformation, NeoplasticCluster AnalysisEnhancer of Zeste Homolog 2 ProteinERG1 Potassium ChannelGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesHistone DemethylasesHumansEnhancer of Zeste Homolog 2 ProteinERG1 Potassium ChannelEZH2 protein, humanHistone DemethylasesKDM1A protein, humanrhoB GTP-Binding ProteinDUXAP8EGR1invasionNSCLCproliferationpseudogeneRHOB

Identifiers

PMID28131418
PMCPMC5363203
OpenAlexW2573592265

What OpenQuestion holds

Textmetadata
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.