Artículos de revistas
Progesterone Receptor Induces ErbB-2 Nuclear Translocation To Promote Breast Cancer Growth via a Novel Transcriptional Effect: ErbB-2 Function as a Coactivator of Stat3
Fecha
2010-12Registro en:
Beguelin, Wendy; Díaz Flaqué, María Celeste; Proietti Anastasi, Cecilia Jazmín; Cayrol, Maria Florencia; Rivas, Martin Alfredo; et al.; Progesterone Receptor Induces ErbB-2 Nuclear Translocation To Promote Breast Cancer Growth via a Novel Transcriptional Effect: ErbB-2 Function as a Coactivator of Stat3; American Society For Microbiology; Molecular And Cellular Biology; 30; 23; 12-2010; 5456-5472
0270-7306
1098-5549
Autor
Beguelin, Wendy
Díaz Flaqué, María Celeste
Proietti Anastasi, Cecilia Jazmín
Cayrol, Maria Florencia
Rivas, Martin Alfredo
Tkach, Mercedes
Rosemblit, Cinthia
Tocci, Johanna Melisa
Charreau, Eduardo Hernan
Schillaci, Roxana
Elizalde, Patricia Virginia
Resumen
Progesterone receptor (PR) and ErbB-2 bidirectional cross talk participates in breast cancer development. Here, we identified a new mechanism of the PR and ErbB-2 interaction involving the PR induction of ErbB-2 nuclear translocation and the assembly of a transcriptional complex in which ErbB-2 acts as a coactivator of Stat3. We also highlighted that the function of ErbB-2 as a Stat3 coactivator drives progestin-induced cyclin D1 promoter activation. Notably, PR is also recruited together with Stat3 and ErbB-2 to the cyclin D1 promoter, unraveling a new and unexpected nonclassical PR genomic mechanism. The assembly of the nuclear Stat3/ErbB-2 transcriptional complex plays a key role in the proliferation of breast tumors with functional PR and ErbB-2. Our findings reveal a novel therapeutic intervention for PR- and ErbB-2-positive breast tumors via the specific blockage of ErbB-2 nuclear translocation.