Document Detail


Role of IL-6 in neuroendocrine differentiation and chemosensitivity of non-small cell lung cancer.
MedLine Citation:
PMID:  15894559     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Interleukin-6 (IL-6) has been shown to regulate both growth and neuroendocrine (NE) differentiation in some types of human cancer cells, and erbB2 may be a critical component of IL-6 signaling. Non-small cell lung cancer (NSCLC) tumors that demonstrate NE properties have been suggested to have biological characteristics similar to small cell lung cancers with initial responsiveness to chemotherapy. We investigated whether IL-6 is implicated in the cell growth, NE differentiation, and chemosensitivity of NSCLC-NE cells. NSCLC-NE cells were treated with exogenous IL-6, and a subclone of an IL-6-transfected NSCLC cell line that constitutively expressed IL-6 receptor was also generated. These cells were assessed for cell proliferation by cell counting and 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assays, chemosensitivity to cisplatin and etoposide by MTT assays, and NE differentiation by observing morphological changes and immunoblotting for neuron-specific enolase (NSE). The IL-6-treated cells and the IL-6-transfected cells showed enhanced cell proliferation and downregulated NSE expression, but little change in chemosensitivity. In the culture medium, IL-6-transfected cells grew as looser aggregates than the parental cells. IL-6 could not activate the erbB genes. In conclusion, IL-6 can induce cell proliferation and NE dedifferentiation but has little effect on chemosensitivity in IL-6 receptor-expressing NSCLC-NE cells. The status of NSE expression is unlikely to be a crucial factor for chemosensitivity in NSCLC cells.
Authors:
Kuo-Ting Chang; Chi-Ying F Huang; Chun-Ming Tsai; Chao-Hua Chiu; Ying-Yung Lok
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-05-13
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  289     ISSN:  1040-0605     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2005 Sep 
Date Detail:
Created Date:  2005-08-11     Completed Date:  2005-09-22     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L438-45     Citation Subset:  IM    
Affiliation:
Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.
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MeSH Terms
Descriptor/Qualifier:
Antineoplastic Agents / pharmacology*
Antineoplastic Agents, Phytogenic / pharmacology
Carcinoma, Non-Small-Cell Lung / metabolism*,  pathology*
Cell Count
Cell Differentiation / drug effects
Cell Division / drug effects
Cell Line, Tumor
Cisplatin / pharmacology
Coloring Agents
Down-Regulation
Etoposide / pharmacology
Humans
Interleukin-6 / metabolism*,  pharmacology
Lung Neoplasms / metabolism*,  pathology*
Neurosecretory Systems / pathology*
Phosphopyruvate Hydratase / metabolism
Receptor, Epidermal Growth Factor / metabolism
Receptors, Interleukin-6 / metabolism
Recombinant Proteins / pharmacology
Signal Transduction
Tetrazolium Salts
Thiazoles
Chemical
Reg. No./Substance:
0/Antineoplastic Agents; 0/Antineoplastic Agents, Phytogenic; 0/Coloring Agents; 0/Interleukin-6; 0/Receptors, Interleukin-6; 0/Recombinant Proteins; 0/Tetrazolium Salts; 0/Thiazoles; 15663-27-1/Cisplatin; 298-93-1/thiazolyl blue; 33419-42-0/Etoposide; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 4.2.1.11/Phosphopyruvate Hydratase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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