NDLI: Combined inhibition of rho-associated protein kinase and EGFR suppresses the invasive phenotype in EGFR-dependent lung cancer cells.

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Combined inhibition of rho-associated protein kinase and EGFR suppresses the invasive phenotype in EGFR-dependent lung cancer cells.

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Combined inhibition of rho-associated protein kinase and EGFR suppresses the invasive phenotype in EGFR-dependent lung cancer cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Umelo, Ijeoma Adaku Wever, Olivier De Kronenberger, Peter Noor, Alfiah Teugels, Erik Chen, Gang Bracke, Marc Grève, Jacques De
Description	Author Affiliation: Umelo IA ( Laboratory of Molecular Oncology and Department of Medical Oncology, Oncologisch Centrum, Universitair Ziekenhuis Brussel, Belgium. Electronic address: iumelo@vub.ac.be.); Wever OD ( Laboratory of Experimental Cancer Research and Department of Radiation Therapy and Experimental Cancer Research, Universitair Ziekenhuis Ghent, Belgium. Electronic address: Olivier.DeWever@UGent.be.); Kronenberger P ( Laboratory of Molecular Oncology and Department of Medical Oncology, Oncologisch Centrum, Universitair Ziekenhuis Brussel, Belgium); Noor A ( Laboratory of Molecular Oncology and Department of Medical Oncology, Oncologisch Centrum, Universitair Ziekenhuis Brussel, Belgium. Electronic address: alfinoor@vub.ac.be.); Teugels E ( Laboratory of Molecular Oncology and Department of Medical Oncology, Oncologisch Centrum, Universitair Ziekenhuis Brussel, Belgium. Electronic address: Erik.Teugels@uzbrussel.be.); Chen G ( Laboratory of Molecular Oncology and Department of Medical Oncology, Oncologisch Centrum, Universitair Ziekenhuis Brussel, Belgium. Electronic address: gangchen@vub.ac.be.); Bracke M ( Laboratory of Experimental Cancer Research and Department of Radiation Therapy and Experimental Cancer Research, Universitair Ziekenhuis Ghent, Belgium. Electronic address: Marc1.Bracke@UGent.be.); Grève JD ( Laboratory of Molecular Oncology and Department of Medical Oncology, Oncologisch Centrum, Universitair Ziekenhuis Brussel, Belgium. Electronic address: Jacques.Degreve@uzbrussel.be.)
Abstract	INTRODUCTION: Lung cancer remains the leading cause of cancer-related mortality worldwide, with metastatic disease frequently a prominent feature at the time of diagnosis. The role of NSCLC-derived EGFR mutations in cancer cell proliferation and survival has been widely reported, but little is known about the function of these mutations in invasive growth and metastasis. In this study, we sought to evaluate the intrinsic invasive properties of NSCLC cells with differing EGFR status and examine possible therapeutic targets that can abrogate invasive growth. MATERIALS AND METHODS: Collagen-based assays and 3D cell cultures were used to assess morphological features, actin cytoskeleton dynamics and the invasive capacity of NSCLC cell lines with differing EGFR status. The role of the RhoA/ROCK/MYPT1 and EGFR/HER pathways in NSCLC-related invasion was investigated by pharmacological inhibition and RNA interference techniques. RESULTS: We demonstrate a positive correlation between EGFR mutational/amplification status and invasive capacity. Knockdown of wild-type and mutant EGFR leads to depletion of active and total MYPT1 levels. Combined pharmacological inhibition or genetic ablation of ROCK/EGFR suppresses the hallmarks of cancer cells and abrogates the invasive phenotype in EGFR-dependent NSCLC cells. CONCLUSIONS: These observations suggest that combined targeting of the ROCK and EGFR/HER pathways may be a potential therapeutic approach in limiting invasive growth in NSCLC.
File Format	HTM / HTML
ISSN	01695002
Issue Number	2
Volume Number	90
e-ISSN	18728332
Journal	Lung Cancer
Language	English
Publisher	Elsevier
Publisher Date	2015-11-01
Publisher Place	Ireland
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Oncology Lung Neoplasms Drug Therapy Neoplasm Invasiveness Prevention & Control Protein Kinase Inhibitors Pharmacology Receptor, Epidermal Growth Factor Antagonists & Inhibitors Rho-associated Kinases Carcinoma, Non-small-cell Lung Metabolism Cell Line, Tumor Cell Proliferation Drug Effects Humans Mutation Phenotype Signal Transduction Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Pulmonary and Respiratory Medicine Cancer Research Oncology

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