TEL, a putative tumor suppressor, induces apoptosis and represses transcription of Bcl-XL

Irvin, Brenda J., Wood, Lauren D., Wang, Lilin, Fenrick, Randy, Sansam, Courtney G., Packham, Graham, Kinch, Michael, Yang, Elizabeth and Hiebert, Scott W. (2003) TEL, a putative tumor suppressor, induces apoptosis and represses transcription of Bcl-XL. Journal of Biological Chemistry, 278, (47), 46378-46386. (doi:10.1074/jbc.M305189200).


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The ETS family transcriptional repressor TEL is frequently disrupted by chromosomal translocations, including the t(12;21) in which the second allele of TEL is deleted in up to 90% of the cases. Consistent with its role as a putative tumor suppressor, TEL expression inhibits colony formation by Ras-transformed NIH 3T3 cells and hinders proliferation of a variety of cell types. Although we observed no alteration in the cell cycle of TEL-expressing cells, we did find a marked increase in apoptosis of serum-starved TEL-expressing NIH 3T3 cells. This decrease in cell survival required the DNA binding domain of TEL, suggesting that TEL repressed an anti-apoptotic gene. These observations prompted us to search for genes regulated by ETS family proteins that regulate apoptosis. The anti-apoptotic molecule Bcl-XL contains multiple ets-factor binding sites within its promoters, and TEL repressed a Bcl-XL promoter-linked reporter gene. Moreover, the enforced expression of TEL decreased the endogenous expression of both Bcl-XL mRNA and protein. TEL-mediated repression of Bcl-XL likely affects cell survival via regulation of the apoptotic pathway.

Item Type: Article
Digital Object Identifier (DOI): doi:10.1074/jbc.M305189200
Related URLs:
Subjects: Q Science > Q Science (General)
R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Divisions : University Structure - Pre August 2011 > School of Medicine > Cancer Sciences
ePrint ID: 26393
Accepted Date and Publication Date:
Date Deposited: 19 Apr 2006
Last Modified: 31 Mar 2016 11:49

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