ArticleMolecular oncology2018
FBXW7 deletion contributes to lung tumor development and confers resistance to gefitinib therapy.
Article in Molecular oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- mRNA Network: Solution for Tracking Chemotherapy Insensitivity in Small-Cell Lung Cancer.Journal of healthcare engineering · 2021Trial
- The role of the WD40-repeat protein family in cancer.Molecular cancer · 2026Review
- FBXW7 regulates MAP7 through ubiquitination to affect the phenotypic characteristics and paclitaxel sensitivity of paclitaxel-resistant lung adenocarcinoma cells.European journal of medical research · 2025Article
- Functional Mapping of Epigenomic Regulators Uncovers Coordinated Tumor Suppression by the HBO1 and MLL1 Complexes.Cancer discovery · 2025Article
- F-box proteins in cancer: from cancer cells to the tumor microenvironment.Cell communication and signaling : CCS · 2025Review
- Association Between Phosphorylated AXL Expression and Survival in Patients with Gastric Cancer.Journal of clinical medicine · 2024Article
- Molecular insights and clinical implications for the tumor suppressor role of SCFBiochimica et biophysica acta. Reviews on cancer · 2024Review
- The FBXW7-binding sites on FAM83D are potential targets for cancer therapy.Breast cancer research : BCR · 2024Article
- Inhibitors Targeting the F-BOX Proteins.Cell biochemistry and biophysics · 2023Review
- Targeting immune cell types of tumor microenvironment to overcome resistance to PD-1/PD-L1 blockade in lung cancer.Frontiers in pharmacology · 2023Review
- FBXW7 and human tumors: mechanisms of drug resistance and potential therapeutic strategies.Frontiers in pharmacology · 2023Review
- Article
- Ubiquitin-specific protease 35 (USP35) mediates cisplatin-induced apoptosis by stabilizing BIRC3 in non-small cell lung cancer.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Clinical significance of FBXW7 loss of function in human cancers.Molecular cancer · 2022Review
- miR-196a Upregulation Contributes to Gefitinib Resistance through Inhibiting GLTP Expression.International journal of molecular sciences · 2022Article
- A novel circ_MACF1/miR-942-5p/TGFBR2 axis regulates the functional behaviors and drug sensitivity in gefitinib-resistant non-small cell lung cancer cells.BMC pulmonary medicine · 2022Article
- Complex genetic alterations contribute to rapid disease progression in anTranslational cancer research · 2021Article
- Mutation Spectrum ofPathology oncology research : POR · 2021Article
- MicroRNA‑92a promotes non‑small cell lung cancer cell growth by targeting tumor suppressor gene FBXW7.Molecular medicine reports · 2020Article
- miR-4634 augments the anti-tumor effects of RAD001 and associates well with clinical prognosis of non-small cell lung cancer.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gefitinib, an epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI), is an effective treatment for non-small-cell lung cancer (NSCLC) with EGFR activating mutations, but inevitably, the clinical efficacy is impeded by the emergence of acquired resistance. The tumor suppressor gene FBXW7 modulates chemosensitivity in various human cancers. However, its role in EGFR-TKI therapy in NSCLC has not been well studied. Here, we demonstrate that the mice with deficient Fbxw7 have greater susceptibility to urethane-induced lung tumor development. Through analysis of The Cancer Genome Atlas data, we show that deletion of FBXW7 occurs in 30.9% of lung adenocarcinomas and 63.5% of lung squamous cell carcinomas, which significantly leads to decrease in FBXW7 mRNA expression. The reduction in FBXW7 mRNA level is associated with poor overall survival in lung cancer patients. FBXW7 knockdown dramatically promotes epithelial-mesenchymal transition, migration, and invasion in NSCLC cells. Moreover, with silenced FBXW7, EGFR-TKI-sensitive cells become resistant to gefitinib, which is reversed by the mammalian target of rapamycin inhibitor, rapamycin. Furthermore, xenograft mouse model studies show that FBXW7 knockdown enhances tumorigenesis and resistance to gefitinib. Combination of gefitinib with rapamycin treatment suppresses tumor formation of gefitinib-resistant (GR) FBXW7-knockdown cells. In conclusion, our findings suggest that loss of FBXW7 promotes NSCLC progression as well as gefitinib resistance and combination of gefitinib and rapamycin may provide an effective therapy for GR NSCLC.
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