TEL, a Putative Tumor Suppressor, Induces Apoptosis and Represses Transcription of Bcl-XL

Brenda J. Irvin, Lauren D. Wood, Lilin Wang, Randy Fenrick, Courtney G. Sansam, Graham Packham, Michael Kinch, Elizabeth Yang, Scott W. Hiebert

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


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-X L likely affects cell survival via regulation of the apoptotic pathway.

Original languageEnglish
Pages (from-to)46378-46386
Number of pages9
JournalJournal of Biological Chemistry
Issue number47
StatePublished - Nov 21 2003


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