scholarly journals Ligand-activated PPARγ downregulates CXCR4 gene expression through a novel identified PPAR response element and inhibits breast cancer progression

Oncotarget ◽  
2016 ◽  
Vol 7 (40) ◽  
pp. 65109-65124 ◽  
Author(s):  
Daniela Rovito ◽  
Giulia Gionfriddo ◽  
Ines Barone ◽  
Cinzia Giordano ◽  
Fedora Grande ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Response Element ◽  
Ppar Response Element

Osteopontin induces multiple changes in gene expression that reflect the six “hallmarks of cancer” in a model of breast cancer progression

2005 ◽  
Vol 43 (4) ◽  
pp. 225-236 ◽  
Author(s):  
Amy C. Cook ◽  
Alan B. Tuck ◽  
Susan McCarthy ◽  
Joel G. Turner ◽  
Rosalyn B. Irby ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Hallmarks Of Cancer

scholarly journals Identification of new genes associated with breast cancer progression by gene expression analysis of predefined sets of neoplastic tissues

2008 ◽  
Vol 123 (6) ◽  
pp. 1327-1338 ◽  
Author(s):  
Daniela Cimino ◽  
Luca Fuso ◽  
Christian Sfiligoi ◽  
Nicoletta Biglia ◽  
Riccardo Ponzone ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Progression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Breast Cancer Progression ◽  
New Genes ◽  
Neoplastic Tissues

scholarly journals The ubiquitin ligase RNF181 stabilizes ERα and modulates breast cancer progression

Oncogene ◽  
2020 ◽  
Vol 39 (44) ◽  
pp. 6776-6788
Author(s):  
Jian Zhu ◽  
Xin Li ◽  
Peng Su ◽  
Min Xue ◽  
Yifeng Zang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Progression ◽  
Ubiquitin Ligase ◽  
Target Gene ◽  
Endocrine Resistance ◽  
Breast Cancer Progression ◽  
Sequencing Analysis ◽  
Target Gene Expression ◽  
Positive Breast Cancer

Abstract ERα positive breast cancer accounts for 70% of breast malignancies. Compared with ERα negative types, ERα positive breast cancer could be effective controlled by endocrine therapy. However, more than half of the patients will develop endocrine resistance, making it an important clinical issue for breast cancer therapy. Endocrine resistance might be caused by multiple alternations, including the components of ERα signaling, during tumor progression. Thus, it is urgent and necessary to uncover the molecular mechanisms that controls ERα expression and stability to improve breast cancer therapeutics. In our current study, we identifies that the ubiquitin ligase RNF181 stabilizes ERα and facilitates breast cancer progression. The expression of RNF181 is correlated with ERα level in human breast tumors and relates to poor survival in endocrine-treated patients. RNF181 depletion inhibits breast cancer progression in vivo and in vitro, reduces ERα protein level and its target gene expression, such as PS2 and GREB1. Unbiased RNA sequencing analysis indicates RNF181 is necessary for ERα signature gene expression in whole genomic level. Immuno-precipitation assays indicate that RNF181 associates with ERα and promotes its stability possibly via inducing ERα K63-linked poly-ubiquitination. In conclusion, our data implicate a non-genomic mechanism by RNF181 via stabilizing ERα protein controls ERα target gene expression linked to breast cancer progression.

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