ArticleScientific reports2018
Ankyrin Repeat Domain 1 Overexpression is Associated with Common Resistance to Afatinib and Osimertinib in EGFR-mutant Lung Cancer.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 55 citations in OpenAlex.
- Article
- ACTN4 Gene Amplification and Actinin-4 Protein Expression for Osimertinib Efficacy in EGFR-Mutant NSCLC.Cancer science · 2025Article
- Ankrd1 Promotes Lamellipodia Formation and Cell Motility via Interaction with Talin-1 in Clear Cell Renal Cell Carcinoma.International journal of molecular sciences · 2025Article
- DUSP1 Promotes Osimertinib Drug-Tolerant Persistence by Inhibiting MAPK/ERK Signaling in Non-small Cell Lung Cancer.Molecular biotechnology · 2025Article
- Ankyrin repeat domain 1 is dysregulated in keloids and suppresses keloid fibroblast growth, migration, and extracellular matrix deposition.CytoJournal · 2025Article
- Titin gene mutations enhance radiotherapy efficacy via modulation of tumour immune microenvironment in rectum adenocarcinoma.Clinical and translational medicine · 2025Article
- Chitinase 3-like-1 (CHI3L1) in the pathogenesis of epidermal growth factor receptor mutant non-small cell lung cancer.Translational oncology · 2024Article
- Research progress of ankyrin repeat domain 1 protein: an updated review.Cellular & molecular biology letters · 2024Review
- Article
- Defective N-glycosylation of IL6 induces metastasis and tyrosine kinase inhibitor resistance in lung cancer.Nature communications · 2024Article
- Afatinib plus PEM and CBDCA overcome osimertinib resistance in EGFR-mutated NSCLC with high thrombospondin-1 expression.Cancer science · 2024Article
- Dysregulated gene subnetworks in breast invasive carcinoma reveal novel tumor suppressor genes.Scientific reports · 2024Article
- Molecular characterization of ANKRD1 in rhabdomyosarcoma cell lines: expression, localization, and proteasomal degradation.Histochemistry and cell biology · 2024Article
- Phosphoproteomic Analysis Identified Mutual Phosphorylation of FAK and Src as a Mechanism of Osimertinib Resistance inJTO clinical and research reports · 2024Article
- Rel Family Transcription Factor NFAT5 Upregulates COX2 via HIF-1α Activity in Ishikawa and HEC1a Cells.International journal of molecular sciences · 2024Article
- Pan-cancer integrated analysis of ANKRD1 expression, prognostic value, and potential implications in cancer.Scientific reports · 2024Article
- ACADL-YAP axis activity in non-small cell lung cancer carcinogenicity.Cancer cell international · 2024Article
- Increased ANKRD1 Levels in Early Senescence Mediated by RBMS1-ElicitedMolecular and cellular biology · 2024Article
- NRP1 regulates autophagy and proliferation of gastric cancer through Wnt/β-catenin signaling pathway.Aging · 2023Article
- A context-aware deconfounding autoencoder for robust prediction of personalized clinical drug response from cell-line compound screening.Nature machine intelligence · 2022Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overcoming acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is critical in combating EGFR-mutant non-small cell lung cancer (NSCLC). We tried to construct a novel therapeutic strategy to conquer the resistance to second-and third-generation EGFR-TKIs in EGFR-positive NSCLC patients. We established afatinib- and osimertinib-resistant lung adenocarcinoma cell lines. Exome sequencing, cDNA array and miRNA microarray were performed using the established cell lines to discover novel therapeutic targets associated with the resistance to second-and third-generation EGFR-TKIs. We found that ANKRD1 which is associated with the epithelial-mesenchymal transition (EMT) phenomenon and anti-apoptosis, was overexpressed in the second-and third-generation EGFR-TKIs-resistant cells at the mRNA and protein expression levels. When ANKRD1 was silenced in the EGFR-TKIs-resistant cell lines, afatinib and osimertinib could induce apoptosis of the cell lines. Imatinib could inhibit ANKRD1 expression, resulting in restoration of the sensitivity to afatinib and osimertinib of EGFR-TKI-resistant cells. In EGFR-mutant NSCLC patients, ANKRD1 was overexpressed in the tumor after the failure of EGFR-TKI therapy, especially after long-duration EGFR-TKI treatments. ANKRD1 overexpression which was associated with EMT features and anti-apoptosis, was commonly involved in resistance to second-and third-generation EGFR-TKIs. ANKRD1 inhibition could be a promising therapeutic strategy in EGFR-mutant NSCLC patients.
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