ArticleThe American journal of pathology2007
SRC-family kinases are activated in non-small cell lung cancer and promote the survival of epidermal growth factor receptor-dependent cell lines.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.
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Who cites it
87 citing papers in PubMed, 154 citations in OpenAlex.
- A phase II trial of the Src-kinase inhibitor saracatinib after four cycles of chemotherapy for patients with extensive stage small cell lung cancer: NCCTG trial N-0621.Lung cancer (Amsterdam, Netherlands) · 2014Trial
- The use of single-agent dasatinib in molecularly unselected non-small-cell lung cancer patients.Expert opinion on investigational drugs · 2011Trial
- Phase II study of dasatinib in patients with advanced non-small-cell lung cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2010Trial
- Phase I/II study of the Src inhibitor dasatinib in combination with erlotinib in advanced non-small-cell lung cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2010Trial
- Review
- Defining the heterogeneous molecular landscape of lung cancer cell responses to epigenetic inhibition.Communications biology · 2026Article
- A Multi-Omics Analysis of a Mitophagy-Related Signature in Pan-Cancer.International journal of molecular sciences · 2025Article
- YES1 as a potential target to overcome drug resistance in EGFR-deregulated non-small cell lung cancer.Archives of toxicology · 2024Article
- Differential network analysis of ROS1 inhibitors reveals lorlatinib polypharmacology through co-targeting PYK2.Cell chemical biology · 2024Article
- A multiomic investigation of lung adenocarcinoma molecular subtypes.Journal of the Chinese Medical Association : JCMA · 2024Article
- Proscillaridin A inhibits lung cancer cell growth and motility through downregulation of the EGFR-Src-associated pathway.American journal of cancer research · 2023Article
- CSK-mediated signalling by integrins in cancer.Frontiers in cell and developmental biology · 2023Review
- Synthesis and biological activity evaluation of 3-(hetero) arylideneindolin-2-ones as potential c-Src inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Review
- The Pyrazolo[3,4-Biomedicines · 2022Article
- Fluorescence Imaging of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance in Non-Small Cell Lung Cancer.Cancers · 2022Review
- Peruvoside is a novel Src inhibitor that suppresses NSCLC cell growth and motility by downregulating multiple Src-EGFR-related pathways.American journal of cancer research · 2022Article
- Interleukin-1β Induces Tissue Factor Expression in A549 Cells via EGFR-Dependent and -Independent Mechanisms.International journal of molecular sciences · 2021Article
- Hyperphosphorylation of HDAC2 promotes drug resistance in a novel dual drug resistant mouse melanoma cell line model: anAmerican journal of cancer research · 2021Article
- Targeting the Src Pathway Enhances the Efficacy of Selective FGFR Inhibitors in Urothelial Cancers with FGFR3 Alterations.International journal of molecular sciences · 2020Article
27 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The role of Src-family kinases (SFKs) in non-small cell lung cancer (NSCLC) has not been fully defined. Here we addressed this question by examining SFK phosphorylation in NSCLC biopsy samples and using genetic and pharmacological approaches to inhibit SFK expression and activity in cultured NSCLC cells. Immunohistochemical analysis of NSCLC biopsy samples using a Tyr416 phosphorylation-specific, pan-SFK antibody revealed staining in 123 (33%) of 370 tumors. Because c-Src is known to be both an upstream activator and downstream mediator of epidermal growth factor receptor (EGFR), we next investigated SFK phosphorylation in a panel of NSCLC cell lines, including ones that depend on EGFR for survival. The EGFR-dependent NSCLC cell lines HCC827 and H3255 had increased phosphorylation of SFKs, and treatment of these cells with an SFK inhibitor (PP1 or SKI-606) induced apoptosis. PP1 decreased phosphorylation of EGFR, ErbB2, and ErbB3 and strikingly enhanced apoptosis by gefitinib, an EGFR inhibitor. HCC827 cells transfected with c-Src short hairpin RNA exhibited diminished phosphorylation of EGFR and ErbB2 and decreased sensitivity to apoptosis by PP1 or gefitinib. We conclude that SFKs are activated in NSCLC biopsy samples, promote the survival of EGFR-dependent NSCLC cells, and should be investigated as therapeutic targets in NSCLC patients.
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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.