ArticleThe Journal of biological chemistry2011
Nuclear translocation of epidermal growth factor receptor by Akt-dependent phosphorylation enhances breast cancer-resistant protein expression in gefitinib-resistant cells.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
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Who cites it
108 citing papers in PubMed, 191 citations in OpenAlex.
- Sortilin exhibits tumor suppressor-like activity by limiting EGFR transduction function.Oncogene · 2026Article
- EGFR-19del nuclear translocation increases HDAC7 expression inhibiting the Hippo pathway and exacerbating TKI resistance in lung adenocarcinoma.Theranostics · 2026Article
- CK8/18 and Claudin Profile of Female Breast Cancers from Botswana.Breast cancer : basic and clinical research · 2026Article
- LncRNAs as regulators of chemoresistance and chemosensitivity in triple-negative breast cancer.Genetics and molecular biology · 2026Article
- BRG1 (SMARCA4) Status Dictates the Response to EGFR Inhibitors in Wild-Type EGFR Non-Small Cell Lung Cancer.Cancers · 2025Article
- Review
- A Novel DNA Repair-Gene Model to Predict Responses to Immunotherapy and Prognosis in Patients With EGFR-Mutant Non-Small Cell Lung Cancer.Thoracic cancer · 2025Article
- Multimodal omics analysis of the EGFR signaling pathway in non-small cell lung cancer and emerging therapeutic strategies.Oncology research · 2025Review
- Review
- From Bench to Bedside: A Team's Approach to Multidisciplinary Strategies to Combat Therapeutic Resistance in Head and Neck Squamous Cell Carcinoma.Journal of clinical medicine · 2024Review
- Pik3c3 expression profiling in the mouse kidney and its role in proximal tubule cell physiology.American journal of physiology. Cell physiology · 2024Article
- A Non-Canonical p75HER2 Signaling Pathway Underlying Trastuzumab Action and Resistance in Breast Cancer.Cells · 2024Article
- p53 modulates kinase inhibitor resistance and lineage plasticity in NF1-related MPNSTs.Oncogene · 2024Article
- YES1 as a potential target to overcome drug resistance in EGFR-deregulated non-small cell lung cancer.Archives of toxicology · 2024Article
- IL-1RA promotes oral squamous cell carcinoma malignancy through mitochondrial metabolism-mediated EGFR/JNK/SOX2 pathway.Journal of translational medicine · 2023Article
- Role of YES1 signaling in tumor therapy resistance.Cancer innovation · 2023Review
- Nuclear export signal mutation of epidermal growth factor receptor enhances malignant phenotypes of cancer cells.American journal of cancer research · 2023Article
- Nuclear epidermal growth factor receptor as a therapeutic target.Exploration of targeted anti-tumor therapy · 2023Review
- Breast cancer: miRNAs monitoring chemoresistance and systemic therapy.Frontiers in oncology · 2023Review
- Chemotherapeutic Resistance Genes of Breast Cancer Patients - An Overview.Advanced pharmaceutical bulletin · 2022Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 6 countries.
Funding
Abstract
Epidermal growth factor receptor (EGFR), an aberrantly overexpressed or activated receptor-tyrosine kinase in many cancers, plays a pivotal role in cancer progression and has been an attractive target for cancer therapy. Gefitinib and erlotinib, two EGFR-tyrosine kinase inhibitors, have been approved for non-small cell lung cancer. However, durable clinical efficacy of these EGFR inhibitors is severely limited by the emergence of acquired resistance. For example, the expression of breast cancer-resistant protein (BCRP/ABCG2) has been shown to confer acquired resistance of wild-type EGFR (wtEGFR)-expressing cancer cells to gefitinib. However, the underlying molecular mechanisms still remain unclear. Here, we show that wtEGFR expression is elevated in the nucleus of acquired gefitinib-resistant cancer cells. Moreover, nuclear translocation of EGFR requires phosphorylation at Ser-229 by Akt. In the nucleus, EGFR then targets the proximal promoter of BCRP/ABCG2 and thereby enhances its gene transcription. The nuclear EGFR-mediated BCRP/ABCG2 expression may contribute at least in part to the acquired resistance of wtEGFR-expressing cancer cells to gefitinib. Our findings shed light on the role of nuclear EGFR in the sensitivity of wtEGFR-expressing cancer cells to EGFR tyrosine kinase inhibitors and also deciphered a putative molecular mechanism contributing to gefitinib resistance through BCRP/ABCG2 expression.
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Registered trials
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.