Evidence map›Paper›PMID 37156816›Full record

ArticleCell death & disease2023

LncRNA LINC00969 promotes acquired gefitinib resistance by epigenetically suppressing of NLRP3 at transcriptional and posttranscriptional levels to inhibit pyroptosis in lung cancer.

Jiali Dai, Tianyu Qu, Dandan Yin, Yanan Cui, Chen Zhang, Erbao Zhang, Renhua Guo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
14.2field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. PYRIN mActa pharmacologica Sinica · 2026
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  20. LncRNA-Histone Modification Crosstalk: Orchestrating Cancer Pathobiology.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review

7 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

7 authors at 5 institutions in 1 country.

Jiali Dai *Department of Oncology, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, P. R. China.
Tianyu Qu *Department of Respiratory Medicine, Zhongda Hospital of Southeast University, Nanjing, Jiangsu, 210009, P. R. China.
Dandan Yin *Clinical Research Center, The Second Hospital of Nanjing, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210003, P. R. China.
Yanan Cui *Department of Oncology, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, P. R. China.
Chen ZhangDepartment of Oncology, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, P. R. China.
Erbao ZhangDepartment of Epidemiology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, P. R. China. erbaozhang@njmu.edu.cn.ORCID 0000-0002-5752-7976
Renhua GuoDepartment of Oncology, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, 210029, P. R. China. rhguo@njmu.edu.cn.ORCID 0000-0001-9778-1357
Jiangsu Province Hospital · CNJiangsu Cancer Hospital · CNNanjing Medical University · CNNanjing University of Chinese Medicine · CNZhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) treatment prolongs the survival of lung cancer patients harbouring activating EGFR mutations. However, resistance to EGFR-TKIs is inevitable after long-term treatment. Molecular mechanistic research is of great importance in combatting resistance. A comprehensive investigation of the molecular mechanisms underlying resistance has important implications for overcoming resistance. An accumulating body of evidence shows that lncRNAs can contribute to tumorigenesis and treatment resistance. By bioinformatics analysis, we found that LINC00969 expression was elevated in lung cancer cells with acquired gefitinib resistance. LINC00969 regulated resistance to gefitinib in vitro and in vivo. Mechanistically, gain of H3K4me1 and H3K27Ac led to the activation of LINC00969 expression. LINC00969 interacts with EZH2 and METTL3, transcriptionally regulates the level of H3K27me3 in the NLRP3 promoter region, and posttranscriptionally modifies the m6A level of NLRP3 in an m6A-YTHDF2-dependent manner, thus epigenetically repressing NLRP3 expression to suppress the activation of the NLRP3/caspase-1/GSDMD-related classical pyroptosis signalling pathways, thereby endowing an antipyroptotic phenotype and promoting TKI resistance in lung cancer. Our findings provide a new mechanism for lncRNA-mediated TKI resistance from the new perspective of pyroptosis via simultaneous regulation of histone methylation and RNA methylation. The pivotal role of LINC00969 gives it the potential to be a novel biomarker and therapeutic target for overcoming EGFR-TKI resistance in lung cancer.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungLung NeoplasmsRNA, Long NoncodingCell Line, TumorDrug Resistance, NeoplasmErbB ReceptorsGefitinibHumansMethyltransferasesNLR Family, Pyrin Domain-Containing 3 ProteinProtein Kinase InhibitorsPyroptosisQuinazolinesAntineoplastic AgentsErbB ReceptorsGefitinibMethyltransferasesMETTL3 protein, humanNLR Family, Pyrin Domain-Containing 3 ProteinProtein Kinase InhibitorsQuinazolinesRNA, Long Noncoding

Identifiers

PMID37156816
PMCPMC10167249
OpenAlexW4375858578

What OpenQuestion holds

Textmetadata
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.