Skip Navigation



Carcinogenesis Advance Access published online on April 1, 2008
Carcinogenesis, doi:10.1093/carcin/bgn087
This Article
Right arrow Advance Access manuscript (PDF)
Right arrow Supplementary Data
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Kandalaft, L. E.
Right arrow Articles by Jakowlew, S. B.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kandalaft, L. E.
Right arrow Articles by Jakowlew, S. B.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Differentially Expressed Nucleolar TGF-β1 Target (DENTT) exhibits an inhibitory role on tumorigenesis

Lana E. Kandalaft1,*, Enrique Zudaire2,*, Sergio Portal-Núñez2, Frank Cuttitta2 and Sonia B. Jakowlew3

1 Cell and Cancer Biology Branch, National Cancer Institute, Advanced Technology Center, Gaithersburg, MD 20877, USA
2 NCI Angiogenesis Core Facility, National Cancer Institute, Advanced Technology Center, Gaithersburg, MD 20877, USA
3 Cell and Cancer Biology Branch, National Cancer Institute, Rockville, MD, 20850, USA

Corresponding author: Lana E Kandalaft, PhD, Cell and Cancer Biology Branch, National Cancer Institute, Advanced Technology Center, Gaithersburg, MD 20877, USA, Tel. 301-443-4492, E-mail address: kandalal{at}mail.nih.gov

Differentially Expressed Nucleolar TGF-β1 Target (DENTT), also known as Testis-Specific Protein Y-encoded–Like 2 (TSPYL2) and Cell Division Autoantigen-1 (CDA-1), is a member of the TSPY/TSPY-L/SET/NAP-1 protein superfamily. DENTT is expressed in various tissues including normal human lung. Here we investigate the involvement of DENTT in cancer promotion and progression. DENTT mRNA and protein levels were shown to be markedly downregulated in human and mouse primary tumors and in human tumor cell lines. Overexpression of DENTT in human lung (A549-DENTT) and breast (MCF-7-DENTT) cancer cells resulted in diminished growth potential in anchorage-dependent growth assays and reduced capacity to form colonies under anchorage-independent culture conditions. The migratory potential of A549-DENTT and MCF-7-DENTT cells was reduced when compared to empty vector control cells. Treating human lung cell lines with demethylating agents increased DENTT expression significantly. DENTT expression pattern paralleled that of TGF-β1 in normal and malignant tissue and ectopic expression or treatment with TGF-β1 in lung cancer cells was followed by increased DENTT mRNA and protein levels. Collectively, our results suggest a role for DENTT as a suppressor of the tumorigenic phenotype.

* Both authors contributed equally

Received September 17, 2007; revised March 4, 2008; accepted March 24, 2008.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.