| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Biomarkers and Prevention Research Branch, Division of Cancer Prevention and Control [E. S., M. E. R., M. J. B., R. I. L.], and Biostatistics and Data Management Section [S. M. S.], National Cancer Institute, Rockville, Maryland 20850
Although the c-jun oncogene is an integral part of the AP-1 transcriptional complex implicated in the process of tumor promotion, its role in the pathogenesis of human tumors is unknown. We analyzed the expression and function of cJun in 110 non-small cell lung cancer (NSCLC) primary and metastatic tumors, histologically atypical areas from the surrounding lung, and 10 NSCLC cell lines to examine the role of cJun in lung carcinogenesis. cJun was expressed in primary and metastatic lung tumors in 31% of cases, with no association with survival. Whereas normal conducting airway and alveolar epithelia in general did not express cJun by immunohistochemistry, histologically atypical areas were frequently positive for cJun, regardless of the status of the corresponding tumor. Multiple members of the jun and fos gene families were frequently expressed at the mRNA level in vitro, with detectable functional activity (as defined by AP-1-specific DNA binding and/or transactivation of an AP-1-driven reporter construct) present in all 10 NSCLC cell lines examined. Although tumor-promoting phorbol esters had little effect on c-jun expression, serum stimulation generally resulted in significant c-jun induction in NSCLC cell lines. These data show that cJun expression is altered early during human lung carcinogenesis and that cJun may function as a mediator of growth factor signals in NSCLC.
1 To whom requests for reprints should be addressed, at Biomarkers and Prevention Research Branch, Division of Cancer Prevention and Control, National Cancer Institute, 9610 Medical Center Drive, Room 300, Rockville, MD 20850. Phone: (301) 402-3128; Fax: (301) 402-4422; E-mail: szaboe@BPRB.NCI.NIH.GOV.
Received 8/15/95. Accepted 11/ 7/95.
This article has been cited by other articles:
|
|
 |
|
  M. V. Karamouzis, P. A. Konstantinopoulos, and A. G. Papavassiliou The Activator Protein-1 Transcription Factor in Respiratory Epithelium Carcinogenesis Mol. Cancer Res., February 1, 2007; 5(2): 109 - 120. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Lu, J. Liao, G. Yang, K. R. Reuhl, X. Hao, and C. S. Yang Inhibition of Adenoma Progression to Adenocarcinoma in a 4-(Methylnitrosamino)-1-(3-Pyridyl)-1-Butanone-Induced Lung Tumorigenesis Model in A/J Mice by Tea Polyphenols and Caffeine Cancer Res., December 1, 2006; 66(23): 11494 - 11501. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. L. Keith, Y. E. Miller, T. M. Hudish, C. E. Girod, S. Sotto-Santiago, W. A. Franklin, R. A. Nemenoff, T. H. March, S. P. Nana-Sinkam, and M. W. Geraci Pulmonary Prostacyclin Synthase Overexpression Chemoprevents Tobacco Smoke Lung Carcinogenesis in Mice Cancer Res., August 15, 2004; 64(16): 5897 - 5904. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. M. Ardies Inflammation as Cause for Scar Cancers of the Lung Integr Cancer Ther, September 1, 2003; 2(3): 238 - 246. [Abstract] [PDF]
|
|
|
|
 |
|
 S. P. M. Reddy and B. T. Mossman Role and regulation of activator protein-1 in toxicant-induced responses of the lung Am J Physiol Lung Cell Mol Physiol, December 1, 2002; 283(6): L1161 - L1178. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Kakolyris, A. Giatromanolaki, M. Koukourakis, G. Powis, J. Souglakos, E. Sivridis, V. Georgoulias, K. C. Gatter, and A. L. Harris Thioredoxin Expression Is Associated with Lymph Node Status and Prognosis in Early Operable Non-Small Cell Lung Cancer Clin. Cancer Res., October 1, 2001; 7(10): 3087 - 3091. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Shukla, C. R. Timblin, A. K. Hubbard, J. Bravman, and B. T. Mossman Silica-induced Activation of c-Jun-NH2-Terminal Amino Kinases, Protracted Expression of the Activator Protein-1 Proto-Oncogene, fra-1, and S-Phase Alterations Are Mediated via Oxidative Stress Cancer Res., March 1, 2001; 61(5): 1791 - 1795. [Abstract] [Full Text]
|
|
|
|
|
|
H. Wan, W. K. Hong, and R. Lotan Increased Retinoic Acid Responsiveness in Lung Carcinoma Cells that Are Nonresponsive Despite the Presence of Endogenous Retinoic Acid Receptor (RAR) {beta} by Expression of Exogenous Retinoid Receptors Retinoid X Receptor {{alpha}}, RAR{{alpha}}, and RAR{{gamma}} Cancer Res., January 1, 2001; 61(2): 556 - 564. [Abstract] [Full Text]
|
|
|
|
 |
|
 F. Bost, R. McKay, N. Dean, and D. Mercola The JUN Kinase/Stress-activated Protein Kinase Pathway Is Required for Epidermal Growth Factor Stimulation of Growth of Human A549 Lung Carcinoma Cells J. Biol. Chem., December 26, 1997; 272(52): 33422 - 33429. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |
