Evidence map›Paper›PMID 39704929›Full record

ArticleGenes & genomics2025

CKAP4 is a potential therapeutic target to overcome resistance to EGFR-TKIs in lung adenocarcinoma.

Seongeun Song, Sangmyung Rhee

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Article in Genes & genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Seongeun SongDepartment of Life Science, Chung-Ang University, Seoul, 06974, Republic of Korea.
Sangmyung RheeDepartment of Life Science, Chung-Ang University, Seoul, 06974, Republic of Korea. Sangmyung.rhee@cau.ac.kr.

Funding

Korea Institute for Advanced Study RS-2023-00220089Korea Institute for Advanced Study RS-2024-00348828
6 · The paper itself

Abstract

backgroundEpidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are standard treatments for non-small cell lung cancer (NSCLC) patients with EGFR mutations; however, drug resistance limits their efficacy. Cytoskeleton-associated protein 4 (CKAP4) has been linked to cancer progression, but its role in EGFR-TKI resistance remains unclear.

objectiveThis study investigates the clinical relevance of CKAP4 as a therapeutic target to overcome EGFR-TKI resistance in lung adenocarcinoma (LUAD) patients.

methodsGEO datasets were analyzed to identify 24 differentially expressed genes associated with EGFR-TKI resistance, with CKAP4 selected via functional annotation and scoring using the VarElect tool. The prognostic significance of CKAP4 was evaluated using public databases, and its upregulation was confirmed in osimertinib-tolerant H1975 cells through quantitative reverse transcription-polymerase chain reaction.

resultsIntegrated bioinformatics analysis identified CKAP4 as strongly associated with EGFR-TKI resistance. Elevated CKAP4 expression was particularly linked to poorer clinical outcomes in LUAD patients. Notably, osimertinib-tolerant cells exhibited high CKAP4 expression, correlating positively with increased half-maximal inhibitory concentrations of EGFR-TKIs. LUAD patients with upregulated CKAP4 showed significantly reduced overall and relapse-free survival.

conclusionThis study underscores the prognostic value of CKAP4 in EGFR-mutated LUAD and highlights its potential as a therapeutic target to counter EGFR-TKI resistance.

Indexed as

Adenocarcinoma of LungCytoskeletal ProteinsDrug Resistance, NeoplasmLung NeoplasmsProtein Kinase InhibitorsAcrylamidesAniline CompoundsCell Line, TumorErbB ReceptorsGene Expression Regulation, NeoplasticHumansIndolesMutationPrognosisPyrimidinesAcrylamidesAniline CompoundsCytoskeletal ProteinsEGFR protein, humanErbB ReceptorsIndolesosimertinibProtein Kinase InhibitorsPyrimidinesBioinformatics analysisCKAP4EGFR-TKI resistanceNSCLCTherapeutic target

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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.