Evidence map›Paper›PMID 39030638›Full record

ArticleJournal of experimental & clinical cancer research : CR2024

Hypoxia-enhanced YAP1-EIF4A3 interaction drives circ_0007386 circularization by competing with CRIM1 pre-mRNA linear splicing and promotes non-small cell lung cancer progression.

Lixia Li, Dewei Liu, Tingting Chen, Chunhui Wei, Youping Qiao, Weiliang Liu, Yanmei Liang, Zhu Liang, Chunyuan Chen, Dongming Li and 4 more

Abstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

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  5. Hypoxia-induced circ_0017521 enhances glycolysis and promotes NSCLC progression via upregulating the PFKFB3/PI3K-AKT pathway.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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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

14 authors.

Lixia Li *Cancer Hospital, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Dewei Liu *Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China.
Tingting Chen *Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China.
Chunhui WeiDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China.
Youping QiaoDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China.
Weiliang LiuDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China.
Yanmei LiangDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China.
Zhu LiangDepartment of Cardiothoracic Surgery, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Chunyuan ChenDepartment of Cardiothoracic Surgery, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Dongming LiDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China.
Bin WuDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China.
Xuanna ZhaoDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China. 792665234@qq.com.
Dan HuangDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China. 287538250@qq.com.
Dong WuDepartment of Respiratory and Critical Care Medicine, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524000, China. wudong98@126.com.ORCID http://orcid.org/0000-0002-2842-1144

Funding

Affliated Hospital of Guangdong Medical University "Clinical Medicine+" CnTech Co-operation Project LP2021B001, CLP2021B017Affliated Hospital of Guangdong Medical University "Start-up of scientific research funding for high-level talents" 202217Clinical Research Project of Affiliated Hospital of Guangdong Medical University LCYJ2023B003the Basic and Applied Basic Research Programs of Science and Technology Commission Foundation of Guangdong Province 2021A1515011062, 2022A1515011731the Project of Zhanjiang City 2021A05052
6 · The paper itself

Abstract

backgroundThe progression of non-small cell lung cancer (NSCLC) is significantly influenced by circular RNAs (circRNAs), especially in tumor hypoxia microenvironment. However, the precise functions and underlying mechanisms of dysregulated circRNAs in NSCLC remain largely unexplored.

methodsDifferentially expressed circRNAs in NSCLC tissues were identified through high-throughput RNA sequencing. The characteristics of circ_0007386 were rigorously confirmed via Sanger sequencing, RNase R treatment and actinomycin D treatment. The effects of circ_0007386 on proliferation and apoptosis were investigated using CCK8, cloning formation assays, TUNEL staining, and flow cytometry assays in vitro. In vivo, xenograft tumor models were used to evaluate its impact on proliferation. Mechanistically, the regulatory relationships of circ_0007386, miR-383-5p and CIRBP were examined through dual luciferase reporter assays and rescue experiments. Additionally, we detected the binding of EIF4A3 to CRIM1 pre-mRNA by RNA immunoprecipitation and the interaction between YAP1 and EIF4A3 under hypoxic conditions by co-immunoprecipitation.

resultsOur investigation revealed a novel circRNA, designated as circ_0007386, that was upregulated in NSCLC tissues and cell lines. Circ_0007386 modulated proliferation and apoptosis in NSCLC both in vitro and in vivo. Functionally, circ_0007386 acted as a sponge for miR-383-5p, targeting CIRBP, which influenced NSCLC cell proliferation and apoptosis via the PI3K/AKT signaling pathway. Furthermore, under hypoxic conditions, the interaction between YAP1 and EIF4A3 was enhanced, leading to the displacement of EIF4A4 from binding to CRIM1 pre-mRNA. This facilitated the back-splicing of CRIM1 pre-mRNA, increasing the formation of circ_0007386. The circ_0007386/miR-383-5p/CIRBP axis was significantly associated with the clinical features and prognosis of NSCLC patients.

conclusionsCirc_0007386, regulated by YAP1-EIF4A3 interaction under hypoxia conditions, plays an oncogenic role in NSCLC progression via the miR-383-5p/CIRBP axis.

Indexed as

Carcinoma, Non-Small-Cell LungDisease ProgressionEukaryotic Initiation Factor-4ALung NeoplasmsRNA, CircularYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingAnimalsApoptosisCell Line, TumorCell ProliferationDEAD-box RNA HelicasesFemaleGene Expression Regulation, NeoplasticHumansMaleAdaptor Proteins, Signal TransducingDEAD-box RNA HelicasesEIF4A3 protein, humanEukaryotic Initiation Factor-4AMicroRNAsRNA, CircularRNA PrecursorsTranscription FactorsYAP1 protein, humanYAP-Signaling ProteinsApoptosisCIRBPCirc_0007386EIF4A3HypoxiamiR-383-5pNon-small cell lung cancerProliferationYAP1

Identifiers

PMID39030638
PMCPMC11264895

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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.