Evidence map›Paper›PMID 33128099›Full record

ArticleJournal of neuro-oncology2021

LncRNA RP11-84E24.3 drives tumorigenesis and epithelial-to-mesenchymal transition of glioma cells by promoting TFAP2C-mediated activation of SNAI1.

Lisha Chang, Jingyue Wang, Fuling Zhou, Dali Wang, Ruiying Chen, Yunhe Zhang, Jiang Zhang

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Journal of neuro-oncology, 2021. 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 It has been retracted, and should not be counted.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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 40% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Lisha ChangDepartment of Neurology, North China University of Science and Technology Affiliated Hospital, No. 73, Jianshe South Road, Tangshan, 063000, Hebei Province, People's Republic of China.
Jingyue WangDepartment of Neurology, North China University of Science and Technology Affiliated Hospital, No. 73, Jianshe South Road, Tangshan, 063000, Hebei Province, People's Republic of China.
Fuling ZhouDepartment of Neurology, North China University of Science and Technology Affiliated Hospital, No. 73, Jianshe South Road, Tangshan, 063000, Hebei Province, People's Republic of China.
Dali WangDepartment of Neurology, North China University of Science and Technology Affiliated Hospital, No. 73, Jianshe South Road, Tangshan, 063000, Hebei Province, People's Republic of China.
Ruiying ChenDepartment of Neurology, North China University of Science and Technology Affiliated Hospital, No. 73, Jianshe South Road, Tangshan, 063000, Hebei Province, People's Republic of China.
Yunhe ZhangDepartment of Neurosurgery, North China University of Science and Technology Affiliated Hospital, Tangshan, 063000, People's Republic of China.
Jiang ZhangDepartment of Neurology, North China University of Science and Technology Affiliated Hospital, No. 73, Jianshe South Road, Tangshan, 063000, Hebei Province, People's Republic of China. hebeizhangj@163.com.ORCID http://orcid.org/0000-0002-9333-3765
North China University of Science and Technology · CNNorth China University of Science and Technology Affiliated Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeLong noncoding RNAs (LncRNAs) are essential epigenetic regulators with critical roles in tumor initiation and malignant progression; however, the mechanism by which aberrantly expressed lncRNA RP11-84E24.3 regulates the pathogenesis of glioma is not fully understood. Here, we investigate the function of lncRNA RP11-84E24.3 in glioma onset and progression as well as identify a molecular pathway regulated by this lncRNA.

methodsDifferentially expressed lncRNAs related to glioma were identified. The aberrant expression of lncRNA RP11-84E24.3 was verified in samples from patients with glioma as well as glioma cell lines. The role of lncRNA RP11-8424.3 in proliferation, apoptosis, migration, and invasion was assessed using gain- and loss-of function approaches, EdU incorporation, flow cytometry, wound healing and Transwell invasion assays. Western blot analysis was utilized to examine the expression of proteins associated with epithelial-to-mesenchymal transition (EMT). The interaction between lncRNA RP11-84E24.3, TFAP2C and SNAI1 was confirmed using RNA pull-down, ChIP and luciferase reporter assays.

resultsLncRNA RP11-84E24.3 was up-regulated in both glioma tissues and cell lines. LncRNA RP11-84E24.3 overexpression enhanced the proliferation, migration and invasion of glioma cells while reducing apoptosis. This was associated with a decrease in E-cadherin expression and an increase in N-cadherin and Vimentin expression. LncRNA RP11-84E24.3 directly targeted TFAP2C protein, resulting in increased SNAI1 expression. Knockdown of TFAP2C or SNAI1 reversed the effects of lncRNA RP11-84E24.3 overexpression, while silencing lncRNA RP11-84E24.3 inhibited tumor formation of glioma cells in vivo.

conclusionsLncRNA RP11-84E24.3 increased SNAI1 expression by forming a complex with TFAP2C protein, promoting EMT in glioma cells and tumor formation.

Indexed as

Epithelial-Mesenchymal TransitionAdultAnimalsApoptosisBiomarkers, TumorCarcinogenesisCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticGliomaHumansMaleMiceMice, NudeMiddle AgedBiomarkers, TumorRNA, Long NoncodingSNAI1 protein, humanSnail Family Transcription FactorsTFAP2C protein, humanTranscription Factor AP-2Epithelial-to-mesenchymal transitionLong noncoding RNA RP11-84E24.3SNAI1 signaling pathwayTFAP2CU251MG glioma cell

Identifiers

PMID33128099
OpenAlexW3096590237

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.