Evidence map›Paper›PMID 32329150›Full record

ArticleJournal of cellular and molecular medicine2020

SOX9-activated PXN-AS1 promotes the tumorigenesis of glioblastoma by EZH2-mediated methylation of DKK1.

Hongjin Chen, Guoqiang Hou, Jian Yang, Weilin Chen, Liemei Guo, Qin Mao, Jianwei Ge, Xiaohua Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 59 citations in OpenAlex.

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  17. Non-Coding RNAs and Brain Tumors: Insights Into Their Roles in Apoptosis.Frontiers in cell and developmental biology · 2021
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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

8 authors at 2 institutions in 1 country.

Hongjin ChenDepartment of Neurosurgery, School of Medicine, Renji Hospital, Jiaotong University, Shanghai, China.
Guoqiang HouDepartment of Neurosurgery, School of Medicine, Renji Hospital, Jiaotong University, Shanghai, China.
Jian YangDepartment of Pediatric Neurosurgery, Xin Hua Hospital affiliated to School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Weilin ChenDepartment of Neurosurgery, School of Medicine, Renji Hospital, Jiaotong University, Shanghai, China.
Liemei GuoDepartment of Neurosurgery, School of Medicine, Renji Hospital, Jiaotong University, Shanghai, China.
Qin MaoDepartment of Neurosurgery, School of Medicine, Renji Hospital, Jiaotong University, Shanghai, China.
Jianwei GeDepartment of Neurosurgery, School of Medicine, Renji Hospital, Jiaotong University, Shanghai, China.ORCID 0000-0002-5420-2316
Xiaohua ZhangDepartment of Neurosurgery, School of Medicine, Renji Hospital, Jiaotong University, Shanghai, China.
Renji Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence has validated the essential regulation of long non-coding RNAs (lncRNAs) in the biological process of tumours. LncRNA PXN-AS1 has been discovered to be as a tumour suppressor in pancreatic cancer; however, its function and mechanism remain greatly unknown in glioblastoma (GBM). Our present study indicated that PXN-AS1 was highly expressed in GBM tissues and cells. Besides, the knock-down of PXN-AS1 was closely associated with the inhibitory proliferation and inducing apoptosis of GBM cells. PXN-AS1 inhibition was also found to restrain GBM tumour growth. Importantly, SOX9 functioned as a transcription factor and activated PXN-AS1 expression, and overexpressed PXN-AS1 rescued the inhibitory role of down-regulated SOX9 in GBM cell growth. Subsequently, it was discovered that PXN-AS1 activated Wnt/β-catenin pathway. DKK1 was widely known as an inhibitor gene of Wnt/β-catenin pathway, and its expression was negatively associated with PXN-AS1 and SOX9. Interestingly, we found that PXN-AS1 could recruit EZH2 to mediate the H3K27me3 level of DKK1 promoter. Restoration experiments manifested that DKK1 knock-down counteracted PXN-AS1 depletion-mediated repression in GBM cell growth. All facts pointed out that PXN-AS1 might be of importance in exploring the therapeutic strategies of GBM.

Indexed as

AnimalsApoptosisBase SequenceBrain NeoplasmsCarcinogenesisCell Line, TumorCell ProliferationDisease ProgressionEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticGene Expression Regulation, NeoplasticGene SilencingGlioblastomaHumansIntercellular Signaling Peptides and ProteinsMaleDKK1 protein, humanEnhancer of Zeste Homolog 2 ProteinIntercellular Signaling Peptides and ProteinsPXN-AS1 non-coding RNA, humanRNA, Long NoncodingSOX9 Transcription FactorDKK1EZH2glioblastomaPXN-AS1WNT pathway

Identifiers

PMID32329150
PMCPMC7294137
OpenAlexW3019739222

What OpenQuestion holds

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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.