Evidence map›Paper›PMID 30037656›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2018

LINC00470 Coordinates the Epigenetic Regulation of ELFN2 to Distract GBM Cell Autophagy.

Changhong Liu, Haijuan Fu, Xiaoping Liu, Qianqian Lei, Yan Zhang, Xiaoling She, Qiang Liu, Qing Liu, Yingnan Sun, Guiyuan Li and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

45 citing papers in PubMed, 73 citations in OpenAlex.

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  11. Regulation of autophagy by non-coding RNAs in human glioblastoma.Medical oncology (Northwood, London, England) · 2024
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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

11 authors at 6 institutions in 1 country.

Changhong LiuHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, Hunan, China; Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Haijuan FuHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, Hunan, China; Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Xiaoping LiuGuangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510623, Guangdong, China.
Qianqian LeiDepartment of Pathology, Zhengzhou University People's Hospital & Henan Provincial People's Hospital, Zhengzhou 450000, Henan, China.
Yan ZhangCancer Research Institute, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Xiaoling SheSecond Xiangya Hospital, Central South University, Changsha 410013, Hunan, China.
Qiang LiuThird Xiangya Hospital, Central South University, Changsha 410013, Hunan, China.
Qing LiuXiangya Hospital, Central South University, Changsha 410013, Hunan, China.
Yingnan SunHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, Hunan, China.
Guiyuan LiHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, Hunan, China; Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China.
Minghua WuHunan Cancer Hospital and The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha 410013, Hunan, China; Cancer Research Institute, School of Basic Medical Science, Central South University, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha 410078, Hunan, China; Key Laboratory of Carcinogenesis, Ministry of Health, Changsha 410078, Hunan, China. Electronic address: wuminghua554@aliyun.com.
Central South University · CNGuangzhou Medical University · CNSecond Xiangya Hospital of Central South University · CNThird Xiangya Hospital · CNXiangya Hospital Central South University · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epigenetics and genomics of glioblastoma (GBM) are complicated. Previous reports indicate that ELFN2 is widely distributed in the cerebral cortex neurons, striatum, and hippocampus cone and in granular cells. However, the function and mechanism of ELFN2, particularly in GBM, have rarely been explored. In this study, we identified ELFN2 as a new hypomethylation gene that acts as an oncogene in GBM. ELFN2 promoted cell autophagy by interacting with AurkA and eIF2α and inhibiting the activation of AurkA. We also demonstrated that aberrantly high ELFN2 expression is obtained due to hypomethylation of its promoter and abnormal miR-101 and LINC00470 expression in GBM. LINC00470 not only enhanced the expression of ELFN2 through adsorption of miR-101 but also affected the methylation level of ELFN2 by decreasing H3K27me3 occupancy. In addition, LINC00470 played a dominant role in the regulation of GBM cell autophagy, even though it upregulated ELFN2 expression. The results indicate that the combination of LINC00470 and ELFN2 has important significance for evaluating the prognosis of astrocytoma patients.

Indexed as

Aurora Kinase AAutophagyCell Line, TumorDNA MethylationEpigenesis, GeneticGene Expression Regulation, NeoplasticGlioblastomaHumansIn Vitro TechniquesMicroRNAsPromoter Regions, GeneticRNA, Long NoncodingAURKA protein, humanAurora Kinase AMicroRNAsMIRN101 microRNA, humanRNA, Long NoncodingAurkAcell autophagylong noncoding RNAmethylation modificationmiR-101

Identifiers

PMID30037656
PMCPMC6127511
OpenAlexW2809352418

What OpenQuestion holds

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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.