HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 289/3/L438    most recent 00033.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Chang, K.-T. Articles by Lok, Y.-Y. Search for Related Content PubMed PubMed Citation Articles by Chang, K.-T. Articles by Lok, Y.-Y.

Role of IL-6 in neuroendocrine differentiation and chemosensitivity of non-small cell lung cancer

¹Graduate Institute of Life Sciences, National Defense Medical Center, Taipei; ²Division of Molecular and Genomic Medicine, National Health Research Institutes, Miaoli; and ³Section of Thoracic Oncology, Chest Department, Taipei Veterans General Hospital, and Department of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan, Republic of China

Submitted 19 January 2005 ; accepted in final form 5 May 2005

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.

interleukin-6

This article has been cited by other articles:

				H. Dalwadi, K. Krysan, N. Heuze-Vourc'h, M. Dohadwala, D. Elashoff, S. Sharma, N. Cacalano, A. Lichtenstein, and S. Dubinett Cyclooxygenase-2-Dependent Activation of Signal Transducer and Activator of Transcription 3 by Interleukin-6 in Non-Small Cell Lung Cancer Clin. Cancer Res., November 1, 2005; 11(21): 7674 - 7682. [Abstract] [Full Text] [PDF]

				K.-T. Chang, C.-M. Tsai, Y.-C. Chiou, C.-H. Chiu, K.-S. Jeng, and C.-Y. F. Huang IL-6 induces neuroendocrine dedifferentiation and cell proliferation in non-small cell lung cancer cells Am J Physiol Lung Cell Mol Physiol, September 1, 2005; 289(3): L446 - L453. [Abstract] [Full Text] [PDF]