Molecular mechanism of suppression of MDR1 by puerarin from Pueraria lobata via NF-κB pathway and cAMP-responsive element transcriptional activity-dependent up-regulation of AMP-activated protein kinase in breast cancer MCF-7/adr cells

2010 ◽  
Vol 54 (7) ◽  
pp. 918-928 ◽  
Author(s):  
Tran Thi Hien ◽  
Hyung Gyun Kim ◽  
Eun Hee Han ◽  
Keon Wook Kang ◽  
Hye Gwang Jeong
Keyword(s):  
Breast Cancer ◽  
Protein Kinase ◽  
Molecular Mechanism ◽  
Transcriptional Activity ◽  
Pueraria Lobata ◽  
Responsive Element ◽  
Amp Activated Protein Kinase ◽  
Activity Dependent ◽  
Mcf 7

Ginseng saponin metabolite induces apoptosis in MCF-7 breast cancer cells through the modulation of AMP-activated protein kinase

2010 ◽  
Vol 30 (2) ◽  
pp. 134-140 ◽  
Author(s):  
Areum Daseul Kim ◽  
Kyoung Ah Kang ◽  
Rui Zhang ◽  
Chae Moon Lim ◽  
Hee Sun Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Ginseng Saponin ◽  
Amp Activated Protein Kinase ◽  
Mcf 7

Celastrol suppresses breast cancer MCF-7 cell viability via the AMP-activated protein kinase (AMPK)-induced p53–polo like kinase 2 (PLK-2) pathway

2013 ◽  
Vol 25 (4) ◽  
pp. 805-813 ◽  
Author(s):  
Ji Hae Kim ◽  
Jung Ok Lee ◽  
Soo Kyung Lee ◽  
Nami Kim ◽  
Ga Young You ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Protein Kinase ◽  
Cell Viability ◽  
Amp Activated Protein Kinase ◽  
Mcf 7

scholarly journals Real-Time Challenging of ERα Y537S Mutant Transcriptional Activity in Living Cells

Endocrines ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 54-64
Author(s):  
Manuela Cipolletti ◽  
Sara Pescatori ◽  
Filippo Acconcia
Keyword(s):  
Cell Line ◽  
Transcriptional Activity ◽  
Estrogen Receptor Α ◽  
Living Cells ◽  
Patient Treatment ◽  
Estrogen Responsive Element ◽  
Specific Proteins ◽  
Responsive Element ◽  
Mcf 7

Metastatic estrogen receptor α (ERα)-expressing breast cancer (BC) occurs after prolonged patient treatment with endocrine therapy (ET) (e.g., aromatase inhibitors—AI; 4OH-tamoxifen—4OH-Tam). Often these metastatic BCs express a mutated ERα variant (e.g., Y537S), which is transcriptionally hyperactive, sustains uncontrolled proliferation, and renders tumor cells insensitive to ET drugs. Therefore, new molecules blocking hyperactive Y537S ERα mutation transcriptional activity are requested. Here we generated an MCF-7 cell line expressing the Y537S ERα mutation stably expressing an estrogen-responsive element (ERE) promoter, which activity can be monitored in living cells. Characterization of this cell line shows both hyperactive basal transcriptional activity with respect to normal MCF-7 cells, which stably express the same ERE-based promoter and a decreased effect of selective ER downregulators (SERDs) in reducing Y537S ERα mutant transcriptional activity with respect to wild type ERα transcriptional activity. Kinetic profiles of Y537S ERα mutant-based transcription produced by both drugs inducing receptor degradation and siRNA-mediated depletion of specific proteins (e.g., FOXA1 and caveolin1) reveals biphasic dynamics of the inhibition of the receptor-regulated transcriptional effects. Overall, we report a new model where to study the behavior of the Y537S ERα mutant that can be used for the identification of new targets and pathways regulating the Y537S ERα transcriptional activity.

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