scholarly journals Analysis of the acute E74 like ETS transcription factor 5 (ELF5)-dependent transcriptome in the mouse mammary tumor virus-Polyoma Middle T (PyMT/ELF5) model of luminal breast cancer

2017 ◽  
Author(s):  
D Gallego-Ortega ◽  
A Ledger ◽  
DL Roden ◽  
AM Law ◽  
A Magenau ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Luminal Breast Cancer ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Ets Transcription Factor

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.

A Mouse Mammary Tumor Virus-Like Long Terminal Repeat Superantigen in Human Breast Cancer

2004 ◽  
Vol 64 (12) ◽  
pp. 4105-4111 ◽  
Author(s):  
Yue Wang ◽  
Jian-Dong Jiang ◽  
Dongping Xu ◽  
Yan Li ◽  
Chunfeng Qu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Long Terminal Repeat ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Human Breast Cancer ◽  
Terminal Repeat ◽  
Human Breast ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

scholarly journals No association between Epstein-Barr Virus and Mouse Mammary Tumor Virus with Breast Cancer in Mexican Women

2013 ◽  
Vol 3 (1) ◽  
Author(s):  
Abigail Morales-Sánchez ◽  
Tzindilú Molina-Muñoz ◽  
Juan L. E. Martínez-López ◽  
Paulina Hernández-Sancén ◽  
Alejandra Mantilla ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Epstein Barr Virus ◽  
Mexican Women ◽  
Mammary Tumor Virus ◽  
Barr Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Epstein Barr

Increased incidence of mouse mammary tumor virus-related antigen in tunisian patients with breast cancer

1984 ◽  
Vol 33 (3) ◽  
pp. 305-308 ◽  
Author(s):  
P. H. Levine ◽  
R. Mesa-Tejada ◽  
I. Keydar ◽  
F. Tabbane ◽  
S. Spiefelman ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tunisian Patients ◽  
Tumor Virus

scholarly journals Stably integrated mouse mammary tumor virus long terminal repeat DNA requires the octamer motifs for basal promoter activity

1994 ◽  
Vol 14 (2) ◽  
pp. 1191-1203
Author(s):  
E Buetti
Keyword(s):  
Transcription Factor ◽  
Transcription Factors ◽  
Long Terminal Repeat ◽  
Binding Site ◽  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Dna Templates ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus

In the mouse mammary tumor virus promoter, a tandem of octamer motifs, recognized by ubiquitous and tissue-restricted Oct transcription factors, is located upstream of the TATA box and next to a binding site for the transcription factor nuclear factor I (NF-I). Their function was investigated with mutant long terminal repeats under different transfection conditions in mouse Ltk- cells and quantitative S1 nuclease mapping of the transcripts. In stable transfectants, which are most representative of the state of proviral DNA with respect to both number of integrated DNA templates and chromatin organization, a long terminal repeat mutant of both octamer sites showed an average 50-fold reduction of the basal transcription level, while the dexamethasone-stimulated level was unaffected. DNase I in vitro footprinting assays with L-cell nuclear protein extracts showed that the mutant DNA was unable to bind octamer factors but had a normal footprint in the NF-I site. I conclude that mouse mammary tumor virus employs the tandem octamer motifs of the viral promoter, recognized by the ubiquitous transcription factor Oct-1, for its basal transcriptional activity and the NF-I binding site, as previously shown, for glucocorticoid-stimulated transcription. A deletion mutant with only one octamer site showed a marked base-level reduction at high copy number but little reduction at low copies of integrated plasmids. The observed transcription levels may depend both on the relative ratio of transcription factors to DNA templates and on the relative affinity of binding sites, as determined by oligonucleotide competition footprinting.

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