scholarly journals Loss of the E3 ubiquitin ligase HACE1 results in enhanced Rac1 signaling contributing to breast cancer progression

Oncogene ◽  
2015 ◽  
Vol 34 (42) ◽  
pp. 5395-5405 ◽  
Author(s):  
E T Goka ◽  
M E Lippman
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Breast Cancer Progression

scholarly journals Atypical ubiquitin ligase RNF31: the nuclear factor modulator in breast cancer progression

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Jian Zhu ◽  
Ting Zhuang ◽  
Huijie Yang ◽  
Xin Li ◽  
Huandi Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Ubiquitin Ligase ◽  
Breast Cancer Progression ◽  
Nuclear Factor

scholarly journals RNF167 activates mTORC1 and promotes tumorigenesis by targeting CASTOR1 for ubiquitination and degradation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Tingting Li ◽  
Xian Wang ◽  
Enguo Ju ◽  
Suzane Ramos da Silva ◽  
Luping Chen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Ubiquitin Ligase ◽  
E3 Ubiquitin Ligase ◽  
Cell Types ◽  
Alternative Mechanism ◽  
Central Controller ◽  
Low Levels ◽  
Mtorc1 Activation

AbstractmTORC1, a central controller of cell proliferation in response to growth factors and nutrients, is dysregulated in cancer. Whereas arginine activates mTORC1, it is overridden by high expression of cytosolic arginine sensor for mTORC1 subunit 1 (CASTOR1). Because cancer cells often encounter low levels of nutrients, an alternative mechanism might exist to regulate CASTOR1 expression. Here we show K29-linked polyubiquitination and degradation of CASTOR1 by E3 ubiquitin ligase RNF167. Furthermore, AKT phosphorylates CASTOR1 at S14, significantly increasing its binding to RNF167, and hence its ubiquitination and degradation, while simultaneously decreasing its affinity to MIOS, leading to mTORC1 activation. Therefore, AKT activates mTORC1 through both TSC2- and CASTOR1-dependent pathways. Several cell types with high CASTOR1 expression are insensitive to arginine regulation. Significantly, AKT and RNF167-mediated CASTOR1 degradation activates mTORC1 independent of arginine and promotes breast cancer progression. These results illustrate a mTORC1 regulating mechanism and identify RNF167 as a therapeutic target for mTORC1-dysregulated diseases.

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.

Beta haemoglobin (hbb) is a novel marker of breast cancer progression

2014 ◽  
Author(s):  
Mattia Capulli ◽  
Adriano Angelucci ◽  
Anna Teti ◽  
Patrizia Sanita ◽  
Luca Ventura ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Breast Cancer Progression
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