ArticleCell death & disease2018
RNF25 promotes gefitinib resistance in EGFR-mutant NSCLC cells by inducing NF-κB-mediated ERK reactivation.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- The methylation pattern of osimertinib resistance: prospects for diagnosis and treatment of NSCLC.Frontiers in oncology · 2026Review
- The STAT3-ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer.Frontiers in oncology · 2026Article
- RNF25 serves as a novel diagnostic and prognostic biomarker in multiple myeloma: a multi-cohort integrative analysis.Hereditas · 2025Article
- The RING finger E3 ligase RNF25 protects DNA replication forks independently of its canonical roles in ubiquitin signaling.Nature communications · 2025Article
- The RING Finger E3 Ligase RNF25 Protects DNA Replication Forks Independently of its Canonical Roles in Ubiquitin Signaling.bioRxiv : the preprint server for biology · 2025Article
- LPIN1 Induces Gefitinib Resistance in EGFR Inhibitor-Resistant Non-Small Cell Lung Cancer Cells.Cancers · 2022Article
- The Systematic Analyses of RING Finger Gene Signature for Predicting the Prognosis of Patients with Hepatocellular Carcinoma.Journal of oncology · 2022Article
- Tumor immune microenvironment in epidermal growth factor receptor-mutated non-small cell lung cancer before and after epidermal growth factor receptor tyrosine kinase inhibitor treatment: a narrative review.Translational lung cancer research · 2021Review
- Lentivirus-mediated silencing of CNTN1 enhances gefitinib sensitivity by reversing epithelial-mesenchymal transition in lung adenocarcinoma A549 cells.Oncology letters · 2021Article
- DGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway.Experimental & molecular medicine · 2021Article
- Identification of HIPK3 as a potential biomarker and an inhibitor of clear cell renal cell carcinoma.Aging · 2021Article
- Overexpression of CTEN is associated with gefitinib resistance in non-small cell lung cancer.Oncology letters · 2021Article
- Hypoxia Induces Resistance to EGFR Inhibitors in Lung Cancer Cells via Upregulation of FGFR1 and the MAPK Pathway.Cancer research · 2020Article
- Novel regulation of miR-34a-5p and HOTAIR by the combination of berberine and gefitinib leading to inhibition of EMT in human lung cancer.Journal of cellular and molecular medicine · 2020Article
- Nuclear Factor κB Signaling and Its Related Non-coding RNAs in Cancer Therapy.Molecular therapy. Nucleic acids · 2020Review
- Identification of a Ubiquitination-Related Gene Risk Model for Predicting Survival in Patients With Pancreatic Cancer.Frontiers in genetics · 2020Article
- Gene Expression Along with Genomic Copy Number Variation and Mutational Analysis Were Used to Develop a 9-Gene Signature for Estimating Prognosis of COAD.OncoTargets and therapy · 2020Article
- Recombinant cell-permeable HOXA9 protein inhibits NSCLC cell migration and invasion.Cellular oncology (Dordrecht, Netherlands) · 2019Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) patients with EGFR mutations initially respond well to EGFR tyrosine kinase inhibitors (TKIs) but eventually exhibit acquired or innate resistance to the therapies typically due to gene mutations, such as EGFR T790M mutation or a second mutation in the downstream pathways of EGFR. Importantly, a significant portion of NSCLC patients shows TKI resistance without any known mechanisms, calling more comprehensive studies to reveal the underlying mechanisms. Here, we investigated a synthetic lethality with gefitinib using a genome-wide RNAi screen in TKI-resistant EGFR-mutant NSCLC cells, and identified RNF25 as a novel factor related to gefitinib resistance. Depletion of RNF25 expression substantially sensitized NSCLC cells to gefitinib treatment, while forced expression of RNF25 augmented gefitinib resistance in sensitive cells. We demonstrated that RNF25 mediates NF-κB activation in gefitinib-treated cells, which, in turn, induces reactivation of ERK signal to cause the drug resistance. We identified that the ERK reactivation occurs via the function of cytokines, such as IL-6, whose expression is transcriptionally induced in a gefitinib-dependent manner by RNF25-mediated NF-κB signals. These results suggest that RNF25 plays an essential role in gefitinib resistance of NSCLC by mediating cross-talk between NF-κB and ERK pathways, and provide a novel target for the combination therapy to overcome TKI resistance of NSCLC.
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