TGF-beta-induced apoptosis is essential for embryonic development and 
mainteanance of adult tissues. Impairment of the apoptotic pathway, regulated by 
TGF-beta, plays a center role in tumorigenesis and manifestations of different 
diseases. TIEG2/KLF11 is a recently identified human TGF-beta-inducible zinc 
finger protein belonging to the family of Sp1/KLF-like transcription factors. In 
human and murine tissues it has been shown that TIEG1 and TIEG2 induce apoptosis 
and inhibit cell growth. Since TGF-beta and Tieg1 are able to induce apoptosis 
in the oligodendroglial cell line OLI-neu, we analysed the ability of TIEG2 to 
mimic the effects observed after treatment with TGF-beta and overexpression of 
Tieg1. Herein we report that TIEG2 induces Caspase3-dependent apoptosis in 
murine OLI-neu cells. Furthermore, we could demonstrate that TIEG2 decreases the 
levels of the anti-apoptotic protein Bcl-X(L) and inhibits transcription driven 
by the Bcl-X(L) promoter. These data suggest that TIEG2 serves as a downstream 
mediator of TGF-beta, bridging TGF-beta-dependent signaling to the intracellular 
pathway of apoptosis.