scholarly journals Mechanisms of primary and secondary estrogen target gene regulation in breast cancer cells

2007 ◽  
Vol 36 (1) ◽  
pp. 76-93 ◽  
Author(s):  
V. Bourdeau ◽  
J. Deschenes ◽  
D. Laperriere ◽  
M. Aid ◽  
J. H. White ◽  
...  
PLoS ONE ◽  
2019 ◽  
Vol 14 (11) ◽  
pp. e0225180 ◽  
Author(s):  
Aisling M. Redmond ◽  
Soleilmane Omarjee ◽  
Igor Chernukhin ◽  
Muriel Le Romancer ◽  
Jason S. Carroll

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Wei-xian Chen ◽  
Ling-yun Xu ◽  
Qi Qian ◽  
Xiao He ◽  
Wen-ting Peng ◽  
...  

d Rhamnose β-hederin (DRβ-H), an active component extracted from the traditional Chinese medicinal plant Clematis ganpiniana, has been reported to be effective against breast cancer. Recent studies have also indicated that the isolated exosomes (D/exo) from docetaxel-resistant breast cancer cells MCF-7 (MCF-7/Doc) were associated with resistance transmission by delivering genetic cargo. However, the relevance of D/exo during DRβ-H exposure remains largely unclear. In the present work, exosomes were characterized by morphology and size distribution. We reinforced the significant role of D/exo in spreading chemoresistance from MCF-7/Doc to recipient sensitive cells after absorption and internalization. DRβ-H could reduce the formation and release of D/exo. Next, we demonstrated that DRβ-H was able to reverse docetaxel resistance and that D/exo was responsible for DRβ-H-mediated resistance reversal. We also found that DRβ-H could decrease the expressions of several most abundant miRNAs (miR-16, miR-23a, miR-24, miR-26a, and miR-27a) transported by D/exo. Target gene prediction and pathway analysis showed the involvement of these selected miRNAs in pathways related to treatment failure. Our results suggested that DRβ-H could reduce D/exo secretion from MCF-7/Doc cells and induce the reduction in resistance transmission via D/exo.


2011 ◽  
Vol 272 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Bing Li ◽  
Xianming Chu ◽  
Meihua Gao ◽  
Yingjie Xu

2016 ◽  
Vol 1859 (11) ◽  
pp. 1389-1397 ◽  
Author(s):  
A. Rasim Barutcu ◽  
Deli Hong ◽  
Bryan R. Lajoie ◽  
Rachel Patton McCord ◽  
Andre J. van Wijnen ◽  
...  

2018 ◽  
Vol 49 (3) ◽  
pp. 1060-1073 ◽  
Author(s):  
Na Song ◽  
Jiateng Zhong ◽  
Qing Hu ◽  
Tengteng Gu ◽  
Bo Yang ◽  
...  

Background/Aims: Fibroblast growth factors (FGFs) and their high-affinity receptors contribute to autocrine and paracrine growth stimulation in several human malignant tumors, including breast cancer. However, the mechanisms underlying the carcinogenic actions of FGF18 remain unclear. Methods: The transcription level of FGF18 under the hypoxic condition was detected with quantitative PCR (qPCR). A wound-healing assay was performed to assess the role of FGF18 in cell migration. A clonogenicity assay was used to determine whether FGF18 silencing affected cell clonogenicity. Western blotting was performed to investigate Akt/GSK3β/β-catenin pathway protein expression. Binding of β-catenin to the target gene promoter was determined by chromatin immunoprecipitation (ChIP) assays. Results: FGF18 promoted the epithelial-mesenchymal transition (EMT) and migration in breast cancer cells through activation of the Akt/GSK3β/β-catenin pathway. FGF18 increased Akt-Ser473 and -Thr308 phosphorylation, as well as that of GSK3β-Ser9. FGF18 also enhanced the transcription of proliferation-related genes (CDK2, CCND2, Ki67), metastasis-related genes (TGF-β, MMP-2, MMP-9), and EMT markers (Snail-1, Snail-2, N-cadherin, vimentin, TIMP1). β-catenin bound to the target gene promoter on the ChIP assay. Conclusion: FGF18 contributes to the migration and EMT of breast cancer cells following activation of the Akt/GSK3β/β-catenin pathway. FGF18 expression may be a potential prognostic therapeutic marker for breast cancer.


2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Keturah Crease ◽  
Colby Williams ◽  
Peng ma ◽  
Elena Skripnikova ◽  
Thomas Wiese

2008 ◽  
Vol 6 (7) ◽  
pp. 82
Author(s):  
D. Schunke ◽  
P. Span ◽  
H. Ronneburg ◽  
A. Dittmer ◽  
M. Vetter ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document