ArticleCarcinogenesis2009
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.
Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- ETS transcription factor ELK3: Molecular insights and translational horizons in cancer (Review).Oncology letters · 2026Review
- Construction of gastric cancer prognostic signature based on the E26 transcription factor and the identification of novel oncogene ELK3.American journal of cancer research · 2024Article
- [Expression characteristics and functional analysis of ELK3 in gastric cancer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
- Prognostic signature composed of transcription factors accurately predicts the prognosis of gastric cancer patients.Cancer cell international · 2021Article
- Transcriptional deregulation underlying the pathogenesis of small cell lung cancer.Translational lung cancer research · 2018Review
- Anti-neoplastic drugs increase caveolin-1-dependent migration, invasion and metastasis of cancer cells.Oncotarget · 2017Article
- The ELK3-GATA3 axis orchestrates invasion and metastasis of breast cancer cells in vitro and in vivo.Oncotarget · 2016Article
- PEA3 transcription factors are downstream effectors of Met signaling involved in migration and invasiveness of Met-addicted tumor cells.Molecular oncology · 2015Article
- Paracrine signaling between tumor subclones of mouse SCLC: a critical role of ETS transcription factor Pea3 in facilitating metastasis.Genes & development · 2015Article
- Increased FGF1-FGFRc expression in idiopathic pulmonary fibrosis.Respiratory research · 2015Article
- ELK3 Expression Correlates With Cell Migration, Invasion, and Membrane Type 1-Matrix Metalloproteinase Expression in MDA-MB-231 Breast Cancer Cells.Gene expression · 2015Article
- Pea3 expression promotes the invasive and metastatic potential of colorectal carcinoma.World journal of gastroenterology · 2014Article
- Elk3 is essential for the progression from progenitor to definitive neural crest cell.Developmental biology · 2013Article
- Underexpression of tumour suppressor LKB1 in clear cell renal cell carcinoma is common and confers growth advantage in vitro and in vivo.British journal of cancer · 2013Article
- The role of Pea3 group transcription factors in esophageal squamous cell carcinoma.The American journal of pathology · 2011Article
- Transcriptional repression of Caveolin-1 (CAV1) gene expression by GATA-6 in bladder smooth muscle hypertrophy in mice and human beings.The American journal of pathology · 2011Article
- Expression of caveolin in trabecular meshwork cells and its possible implication in pathogenesis of primary open angle glaucoma.Molecular vision · 2011Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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, with increased levels in metastatic tumor cells. We have shown previously that transactivation of an erythroblastosis virus-transforming sequence (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. Polyoma virus enhancer activator 3 (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). Chromatin immunoprecipitation-binding assays and small interfering RNA 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.
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