scholarly journals An ultraconserved Hox–Pbx responsive element resides in the coding sequence of Hoxa2 and is active in rhombomere 4

2008 ◽  
Vol 36 (10) ◽  
pp. 3214-3225 ◽  
Author(s):  
Xavier Lampe ◽  
Omar Abdel Samad ◽  
Allan Guiguen ◽  
Christelle Matis ◽  
Sophie Remacle ◽  
...  
Keyword(s):  
Coding Sequence ◽  
Responsive Element ◽  
Rhombomere 4

scholarly journals 17β-Estradiol Inhibits Apoptosis in MCF-7 Cells, Inducing bcl-2 Expression via Two Estrogen-Responsive Elements Present in the Coding Sequence

2000 ◽  
Vol 20 (8) ◽  
pp. 2890-2901 ◽  
Author(s):  
Bruno Perillo ◽  
Annarita Sasso ◽  
Ciro Abbondanza ◽  
Giuseppe Palumbo
Keyword(s):  
Transcriptional Control ◽  
Mrna Level ◽  
Hormone Treatment ◽  
In Vitro Assays ◽  
Coding Region ◽  
Coding Sequence ◽  
17Β Estradiol ◽  
Responsive Element ◽  
Mcf 7

ABSTRACT We have found that 17β-estradiol induces bcl-2transcription in human breast cancer MCF-7 cells. To identifycis-acting elements involved in this regulation, we have analyzed hormone responsiveness of transiently transfected reporter constructs containing the bcl-2 major promoter (P1). Hormone inducibility was observed only when either of two sequences, located within the bcl-2 coding region and showing one and two mutations with respect to the consensus estrogen-responsive element, were inserted downstream from the P1 promoter. Both sequences behaved as enhancers exclusively in cells expressing the estrogen receptor and were able to bind this receptor in in vitro assays. Transfections into MCF-7 cells of plasmids carrying a bcl-2 cDNA fragment which included these two elements revealed that their simultaneous presence resulted in an additive effect on reporter gene activity, whose size resembled the increase of endogenous bcl-2 mRNA level observed in untransfected cells after hormone treatment. Moreover, the identified elements were able to mediate up-regulation ofbcl-2 expression by 17β-estradiol, since exogenousbcl-2 mRNA was induced by hormone challenge of MCF-7 cells transiently transfected with a vector containing the bcl-2coding sequence cloned under the control of a non-estrogen-responsive promoter. Finally, we show that hormone prevention of apoptosis, induced by incubating MCF-7 cells with hydrogen peroxide, was strictly related to bcl-2 up-regulation. Our results indicate that the bcl-2 major promoter does not containcis-acting elements directly involved in transcriptional control by 17β-estradiol and that hormone treatment inhibits programmed cell death in MCF-7 cells, inducing bcl-2expression via two estrogen-responsive elements located within its coding region.

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