Evidence map›Paper›PMID 31815619›Full record

ArticleMolecular cancer2019

Circular RNA circFGFR1 promotes progression and anti-PD-1 resistance by sponging miR-381-3p in non-small cell lung cancer cells.

Peng-Fei Zhang, Xu Pei, Ke-Sang Li, Li-Na Jin, Fei Wang, Jing Wu, Xue-Mei Zhang

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

Article in Molecular cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 148 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
148citing papers in PubMed, 1 pooled it
17.0field-weighted citation impact, top 1% 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

148 citing papers in PubMed, 1 synthesis or guideline pooled it, 279 citations in OpenAlex.

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  13. Circular RNAs: key players in tumor immune evasion.Molecular and cellular biochemistry · 2025
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88 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Peng-Fei ZhangDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xu PeiDepartment of Cardiothoracic Surgery, the Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Ke-Sang LiDepartment of Hematology and Oncology, Hwa Mei Hospital, University of Chinese Academy of Sciences, Zrhejiang, Ningbo, China.
Li-Na JinDepartment of Hematology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Fei WangDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Jing WuDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xue-Mei ZhangDepartment of Oncology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China. tju_zxm@163.com.ORCID 0000-0003-3031-2905
Shanghai East Hospital · CNNanchang University · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundImmune system evasion, distance tumor metastases, and increased cell proliferation are the main reasons for the progression of non-small cell lung cancer (NSCLC) and the death of NSCLC patients. Dysregulation of circular RNAs plays a critical role in the progression of NSCLC; therefore, further understanding the biological mechanisms of abnormally expressed circRNAs is critical to discovering novel, promising therapeutic targets for NSCLC treatment.

methodsThe expression of circular RNA fibroblast growth factor receptor 1 (circFGFR1) in NSCLC tissues, paired nontumor tissues, and cell lines was detected by RT-qPCR. The role of circFGFR1 in NSCLC progression was assessed both in vitro by CCK-8, clonal formation, wound healing, and Matrigel Transwell assays and in vivo by a subcutaneous tumor mouse assay. In vivo circRNA precipitation, RNA immunoprecipitation, and luciferase reporter assays were performed to explore the interaction between circFGFR1 and miR-381-3p.

resultsHere, we report that circFGFR1 is upregulated in NSCLC tissues, and circFGFR1 expression is associated with deleterious clinicopathological characteristics and poor prognoses for NSCLC patients. Forced circFGFR1 expression promoted the migration, invasion, proliferation, and immune evasion of NSCLC cells. Mechanistically, circFGFR1 could directly interact with miR-381-3p and subsequently act as a miRNA sponge to upregulate the expression of the miR-381-3p target gene C-X-C motif chemokine receptor 4 (CXCR4), which promoted NSCLC progression and resistance to anti-programmed cell death 1 (PD-1)- based therapy.

conclusionTaken together, our results suggest the critical role of circFGFR1 in the proliferation, migration, invasion, and immune evasion abilities of NSCLC cells and provide a new perspective on circRNAs during NSCLC progression.

Indexed as

circFGFR1Immune evasionMetastasisNSCLCProliferation

Identifiers

PMID31815619
PMCPMC6900862
OpenAlexW2995976087

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.