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Carcinogenesis Advance Access published online on May 29, 2009
Carcinogenesis, doi:10.1093/carcin/bgp129
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© The Author 2009. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Increased PEA3/E1AF and Decreased Net/Elk-3, both Ets Proteins, Characterize Human NSCLC Progression and Regulate Caveolin-1 Transcription in Calu-1 and NCI-H23 NSCLC Cell Lines

Karin A. Sloan, Hector A. Marquez, Jun Li, Yuxia Cao, Anne Hinds, Carl J. O'Hara, Satinder Kathuria, Maria I. Ramirez, Mary C. Williams and Hasmeena Kathuria

Sloan, Karin; Boston University School of Medicine, Pulmonary Center
Marquez, Hector; Boston University School of Medicine, Medicine
Li, Jun; Boston University School of Medicine, Pulmonary Center
Cao, Yuxia; Boston University School of Medicine, Pulmonary Center
Hinds, Anne; Boston University School of Medicine, Pulmonary Center
O'Hara, Carl; Boston University School of Medicine, Pathology
Kathuria, Satinder; Edward Hines, Jr. VA Hospital, Pathology
Ramirez, Maria; Boston University School of Medicine, Pulmonary Center
Williams, Mary; Boston University School of Medicine, Pulmonary Center
Kathuria, Hasmeena; Boston University School of Medicine, Pulmonary Center

Corresponding Author and Contact Details. kasloan{at}bu.edu, Boston University School of Medicine, Pulmonary Center, R304, 72 E. Concord St., Boston, MA 02118, 617-638-4860

Caveolin-1 protein has been called a "conditional tumor suppressor" because it can either suppress or enhance tumor progression depending on cellular context. Caveolin-1 levels are dynamic in non-small cell lung cancer (NSCLC), with increased levels in metastatic tumor cells. We have previously shown that transactivation of an ETS cis-element enhances caveolin-1 expression in a murine lung epithelial cell line. Based on high sequence homology between the murine and human caveolin-1 promoters, we proposed that ETS proteins might regulate caveolin-1 expression in human lung tumorigenesis. We confirm that caveolin-1 is not detected in well-differentiated primary lung tumors. PEA3, a pro-metastatic ETS protein in breast cancer, is expressed at low levels in well-differentiated tumors and high levels in poorly-differentiated tumors. Conversely, Net, a known ETS repressor, is expressed at high levels in the nucleus of well-differentiated primary tumor cells. In tumor cells in metastatic lymph node sites, caveolin-1 and PEA3 are highly expressed, whereas Net is now expressed in the cytoplasm. We studied transcriptional regulation of caveolin-1 in two human lung cancer cell lines, Calu-1 (high caveolin-1 expressing) and NCI-H23 (low caveolin-1 expressing). ChIP binding assays, and siRNA experiments show that PEA3 is a transcriptional activator in Calu-1 cells and that Net is a transcriptional repressor in NCI-H23 cells. These results suggest that Net may suppress caveolin-1 transcription in primary lung tumors and that PEA3 may activate caveolin-1 transcription in metastatic lymph nodes.

Received November 14, 2008; revised May 15, 2009; accepted May 16, 2009.


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