Evidence map›Paper›PMID 32778129›Full record

ArticleRespiratory research2020

FGL1 regulates acquired resistance to Gefitinib by inhibiting apoptosis in non-small cell lung cancer.

Cuilan Sun, Weiwei Gao, Jiatao Liu, Hao Cheng, Jiqing Hao

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 109 citations in OpenAlex.

  1. Review
  2. Programmed cell death in lung cancer: mechanisms, immune responses, and therapeutics.Apoptosis : an international journal on programmed cell death · 2026
    Review
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8 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Cuilan SunDepartment of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, Anhui, China.
Weiwei GaoDepartment of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, Anhui, China.
Jiatao LiuDepartment of Pharmacy, the First Affiliated Hospital of Anhui Medical University, Hefei, China.
Hao ChengDepartment of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, Anhui, China.
Jiqing HaoDepartment of Oncology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, Anhui, China. haojiqing@ahmu.edu.cn.
First Affiliated Hospital of Anhui Medical University · CNAnhui Medical University · CN

Funding

Anhui Provincial Key Research and Development Program (CN) 1804h08020240
6 · The paper itself

Abstract

backgroundThis study investigated the role of fibrinogen-like protein 1 (FGL1) in regulating gefitinib resistance of PC9/GR non-small cell lung cancer (NSCLC).

methodsThe effect of different concentrations of gefitinib on cell proliferation were evaluated using the CCK-8 assay. FGL1 expression in the normal human bronchial epithelial cell line Beas-2B, as well as four lung tumor cell lines, H1975, A549, PC9, and PC9/GR, was investigated by using western blotting and qRT-PCR. FGL1 was knocked down using small interfering RNA to evaluate the effects of FGL1 on PC9 and PC9/GR. The correlation between FGL1 expression and gefitinib resistance was determined in vitro via CCK-8 and colony formation assays, and flow cytometry and in vivo via flow cytometry and immunohistochemistry.

resultsFGL1 expression was significantly upregulated in non-small cell lung cancer cells with EGFR mutation and higher in the gefitinib-resistant NSCLC cell line PC9/GR than in the gefitinib-sensitive NSCLC cell line PC9. Further, FGL1 expression in PC9 and PC9/GR cells increased in response to gefitinib treatment in a dose-dependent manner. Knockdown of FGL1 suppressed cell viability, reduced the gefitinib IC50 value, and enhanced apoptosis in PC9 and PC9/GR cells upon gefitinib treatment. Mouse xenograft experiments showed that FGL1 knockdown in PC9/GR tumor cells enhanced the inhibitory and apoptosis-inducing actions of gefitinib. The potential mechanism of gefitinib in inducing apoptosis of PC9/GR cells involves inhibition of PARP1 and caspase 3 expression via suppression of FGL1.

conclusionsFGL1 confers gefitinib resistance in the NSCLC cell line PC9/GR by regulating the PARP1/caspase 3 pathway. Hence, FGL1 is a potential therapeutic target to improve the treatment response of NSCLC patients with acquired resistance to gefitinib.

Indexed as

A549 CellsAnimalsAntineoplastic AgentsApoptosisCarcinoma, Non-Small-Cell LungCell SurvivalDrug Resistance, NeoplasmFibrinogenGefitinibHumansLung NeoplasmsMiceMice, Inbred BALB CMice, NudeXenograft Model Antitumor AssaysAntineoplastic AgentsFGL1 protein, humanFibrinogenGefitinibApoptosisEpidermal growth factor receptorFibrinogen-like-protein 1Gefitinib resistanceNon-small cell lung cancer

Identifiers

PMID32778129
PMCPMC7418324
OpenAlexW3047646106

What OpenQuestion holds

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LicenceCC BY
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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.