scholarly journals Transcriptional silencing of the mouse mammary tumor virus promoter through chromatin remodeling is concomitant with histone H1 phosphorylation and histone H3 hyperphosphorylation at M phase

Virology ◽  
2006 ◽  
Vol 346 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Rabindra N. Bhattacharjee ◽  
Trevor K. Archer
Keyword(s):  
Chromatin Remodeling ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Histone H3 ◽  
Transcriptional Silencing ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
M Phase ◽  
Tumor Virus ◽  
Virus Promoter

Effects of Antiandrogens on Chromatin Remodeling and Transcription of the Integrated Mouse Mammary Tumor Virus Promoter

2000 ◽  
Vol 260 (1) ◽  
pp. 160-165 ◽  
Author(s):  
Heinz-Joachim List ◽  
Catharine L. Smith ◽  
Elisabeth Martinez ◽  
Violaine K. Harris ◽  
Mark Danielsen ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

scholarly journals Heregulin Co-opts PR Transcriptional Action Via Stat3 Role As a Coregulator to Drive Cancer Growth

2015 ◽  
Vol 29 (10) ◽  
pp. 1468-1485 ◽  
Author(s):  
Cecilia J. Proietti ◽  
Franco Izzo ◽  
María Celeste Díaz Flaqué ◽  
Rosalía Cordo Russo ◽  
Leandro Venturutti ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Cancer Growth ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Virus Promoter

Abstract Accumulated findings have demonstrated the presence of bidirectional interactions between progesterone receptor (PR) and the ErbB family of receptor tyrosine kinases signaling pathways in breast cancer. We previously revealed signal transducer and activator of transcription 3 (Stat3) as a nodal convergence point between said signaling pathways proving that Stat3 is activated by one of the ErbBs' ligands, heregulin (HRG)β1 via ErbB2 and through the co-option of PR as a signaling molecule. Here, we found that HRGβ1 induced Stat3 recruitment to the promoters of the progestin-regulated cell cycle modulators Bcl-XL and p21CIP1 and also stimulated Stat3 binding to the mouse mammary tumor virus promoter, which carries consensus progesterone response elements. Interestingly, HRGβ1-activated Stat3 displayed differential functions on PR activity depending on the promoter bound. Indeed, Stat3 was required for PR binding in bcl-X, p21CIP1, and c-myc promoters while exerting a PR coactivator function on the mouse mammary tumor virus promoter. Stat3 also proved to be necessary for HRGβ1-induced in vivo tumor growth. Our results endow Stat3 a novel function as a coregulator of HRGβ1-activated PR to promote breast cancer growth. These findings underscore the importance of understanding the complex interactions between PR and other regulatory factors, such as Stat3, that contribute to determine the context-dependent transcriptional actions of PR.

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