Prevention of Breast Cancer Cell Transformation by Blockade of the AP-1 Transcription Factor

2001 ◽  
Author(s):  
Powel H. Brown
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Transformation ◽  
Prevention Of Breast Cancer

scholarly journals RASSF1A Suppresses Estrogen-Dependent Breast Cancer Cell Growth through Inhibition of the Yes-Associated Protein 1 (YAP1), Inhibition of the Forkhead Box Protein M1 (FOXM1), and Activation of Forkhead Box Transcription Factor 3A (FOXO3A)

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2689
Author(s):  
Sven Roßwag ◽  
Gitta Thiede ◽  
Jonathan P. Sleeman ◽  
Sonja Thaler
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Growth ◽  
Breast Cancer Cell Growth ◽  
Forkhead Box ◽  
Cancer Initiation ◽  
And Function

The estrogen receptor alpha (ERα) is expressed by the majority of breast cancers and plays an important role in breast cancer development and tumor outgrowth. Although ERα is well known to be a specific and efficient therapeutic target, the molecular mechanisms that are responsible for the control of ERα expression and function in the context of breast cancer initiation and progression are complex and not completely elucidated. In previous work, we have demonstrated that the tumor suppressor RASSF1A inhibits ERα expression and function in ERα-positive breast cancer cells through an AKT-dependent mechanism. Transcriptional activators such as forkhead box protein M1 (FOXM1) and forkhead transcription factor 3A (FOXO3A) and signaling pathways such as the Hippo pathway are also known to modulate ERα expression and activity. Here we report that RASSF1A acts as an inhibitor of ERα-driven breast cancer cell growth through a complex, hierarchically organized network that initially involves suppression of the Hippo effector Yes-associated protein 1 (YAP1), which is followed by inhibition of AKT1 activity, increased FOXO3A activity as well as a blockade of FOXM1 and ERα expression. Together our findings provide important new mechanistic insights into how the loss of RASSF1A contributes to ERα+ breast cancer initiation and progression.

scholarly journals Akt Blocks Breast Cancer Cell Motility and Invasion through the Transcription Factor NFAT

2006 ◽  
Vol 22 (1) ◽  
pp. 145
Author(s):  
Merav Yoeli-Lerner ◽  
Gary K. Yiu ◽  
Isaac Rabinovitz ◽  
Peter Erhardt ◽  
Sebastien Jauliac ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cell Motility ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Motility ◽  
Transcription Factor Nfat

scholarly journals POU1F1 transcription factor induces metabolic reprogramming and breast cancer progression via LDHA regulation

Oncogene ◽  
2021 ◽  
Author(s):  
Anxo Martínez-Ordoñez ◽  
Samuel Seoane ◽  
Leandro Avila ◽  
Noemi Eiro ◽  
Manuel Macía ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Metabolic Reprogramming ◽  
Migration And Invasion ◽  
Breast Cancer Cell Lines

AbstractMetabolic reprogramming is considered hallmarks of cancer. Aerobic glycolysis in tumors cells has been well-known for almost a century, but specific factors that regulate lactate generation and the effects of lactate in both cancer cells and stroma are not yet well understood. In the present study using breast cancer cell lines, human primary cultures of breast tumors, and immune deficient murine models, we demonstrate that the POU1F1 transcription factor is functionally and clinically related to both metabolic reprogramming in breast cancer cells and fibroblasts activation. Mechanistically, we demonstrate that POU1F1 transcriptionally regulates the lactate dehydrogenase A (LDHA) gene. LDHA catalyzes pyruvate into lactate instead of leading into the tricarboxylic acid cycle. Lactate increases breast cancer cell proliferation, migration, and invasion. In addition, it activates normal-associated fibroblasts (NAFs) into cancer-associated fibroblasts (CAFs). Conversely, LDHA knockdown in breast cancer cells that overexpress POU1F1 decreases tumor volume and [18F]FDG uptake in tumor xenografts of mice. Clinically, POU1F1 and LDHA expression correlate with relapse- and metastasis-free survival. Our data indicate that POU1F1 induces a metabolic reprogramming through LDHA regulation in human breast tumor cells, modifying the phenotype of both cancer cells and fibroblasts to promote cancer progression.

scholarly journals The AP-1 transcription factor regulates breast cancer cell growth via cyclins and E2F factors

Oncogene ◽  
2007 ◽  
Vol 27 (3) ◽  
pp. 366-377 ◽  
Author(s):  
Q Shen ◽  
I P Uray ◽  
Y Li ◽  
T I Krisko ◽  
T E Strecker ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cell Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Growth ◽  
Breast Cancer Cell Growth
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