Evidence map›Paper›PMID 36457025›Full record

ArticleJournal of experimental & clinical cancer research : CR2022

LncRNA ELF3-AS1 inhibits gastric cancer by forming a negative feedback loop with SNAI2 and regulates ELF3 mRNA stability via interacting with ILF2/ILF3 complex.

Dandan Li, Li Shen, Xudong Zhang, Zhen Chen, Pan Huang, Congcong Huang, Shanshan Qin

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.7field-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

40 citing papers in PubMed, 52 citations in OpenAlex.

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  16. Loss of MNX1 Sensitizes Tumors to Cytotoxic T Cells by Degradation of PD-L1 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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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

7 authors at 1 institution in 1 country.

Dandan Li *Department of Stomatology, Taihe Hospital and Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei, P.R. China.
Li Shen *Department of Stomatology, Taihe Hospital and Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei, P.R. China.
Xudong ZhangLaboratory of Tumor biology, Academy of Bio-Medicine Research, Hubei University of Medicine, Shiyan, Hubei, P.R. China.
Zhen ChenLaboratory of Tumor biology, Academy of Bio-Medicine Research, Hubei University of Medicine, Shiyan, Hubei, P.R. China.
Pan HuangLaboratory of Tumor biology, Academy of Bio-Medicine Research, Hubei University of Medicine, Shiyan, Hubei, P.R. China.
Congcong HuangLaboratory of Tumor biology, Academy of Bio-Medicine Research, Hubei University of Medicine, Shiyan, Hubei, P.R. China.
Shanshan QinDepartment of Stomatology, Taihe Hospital and Hubei Key Laboratory of Embryonic Stem Cell Research, School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, Hubei, P.R. China. qinss77@163.com.ORCID http://orcid.org/0000-0002-8527-5278
Hubei University of Medicine · CN

Funding

National Natural Science Foundation of China 81802375National Natural Science Foundation of China 82203829National Natural Science Foundation of China 82273451
6 · The paper itself

Abstract

backgroundThe biological function of lncRNA ELF3-AS1 remains largely unknown in cancers. The cause of SNAI2 overexpression in tumor metastasis remains largely unclear. The molecular mechanisms underlying the high co-expression of antisense lncRNAs and adjacent protein-coding genes remains unclear.

methodsRNA-seq, CHIP and dual-luciferase reporter assay were performed to identify lncRNAs regulated by SNAI2. MicroRNA-seq and RNA-seq studies were conducted to reveal the biological function of ELF3-AS1 in GC. RNA pulldown and CHIRP assays were conducted to identify the protein that interacts with ELF3-AS1.

resultsA total of 123 lncRNAs were identified to be regulated by SNAI2 in GC by RNA sequencing. The ELF3 gene and antisense lncRNA ELF3-AS1 were both transcriptionally repressed by SNAI2 or SNAI1. Down-regulation of ELF3-AS1 and ELF3 predicted poor prognosis in GC. Nuclear localized lncRNA ELF3-AS1 negatively regulated GC cell cycle progression via suppressing G1/S transition and histone synthesis. ELF3-AS1 mainly inhibited GC metastasis by repressing SNAI2 signaling. Additionally, ELF3-AS1 modulated ELF3 mRNA stability by RNA-RNA interaction. The RNA duplexes formed by ELF3 mRNA and lncRNA ELF3-AS1 directly interacted with the double-stranded RNA (dsRNA) binding protein complex ILF2/ILF3 (NF45/NF90). In turn, the ILF2/ILF3 complex dynamically regulated the expression of ELF3-AS1 and ELF3 by affecting the dsRNA stability.

conclusionsThe SNAI2-ELF3-AS1 feedback loop regulates ELF3 expression at transcriptional and post-transcriptional levels and drives gastric cancer metastasis by maintaining SNAI2 overexpression. The ILF2/ILF3 complex plays a critical role in regulating dsRNA stability. In addition, our work provides a direct evidence that head-to-head antisense lncRNAs can share promoters with neighboring coding genes, which make their expression subject to similar transcriptional regulation, leading to high co-expression.

Indexed as

RNA, Long NoncodingStomach NeoplasmsDNA-Binding ProteinsDown-RegulationFeedbackHumansNuclear Factor 45 ProteinNuclear Factor 90 ProteinsProto-Oncogene Proteins c-etsRNA, Double-StrandedRNA StabilitySnail Family Transcription FactorsTranscription FactorsDNA-Binding ProteinsELF3 protein, humanILF2 protein, humanILF3 protein, humanNuclear Factor 45 ProteinNuclear Factor 90 ProteinsProto-Oncogene Proteins c-etsRNA, Double-StrandedRNA, Long NoncodingSNAI2 protein, humanSnail Family Transcription FactorsTranscription FactorsELF3-AS1Gastric cancer metastasismRNA stabilitySNAI2 overexpressionTranscriptional regulation

Identifiers

PMID36457025
PMCPMC9716751
OpenAlexW4310709416

What OpenQuestion holds

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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.