Abstract
SAG is an essential RING component of the Cullin-RING ligase (CRL) E3 ubiquitin ligase complex, which regulates diverse signaling pathways and biological processes, including cell apoptosis, embryonic development, angiogenesis, and tumorigenesis. In the present study, we revealed that SAG gene expression is upregulated in breast cancer cells and that SAG overexpression is associated with significant poorer survival in breast cancer, especially the luminal A subtype. We also detected highly correlated co-overexpression of SAG and COPB2 in breast cancers. Subsequent in vitro experiments demonstrated that SAG and COPB2 act cooperatively to stimulate breast cancer cell proliferation, migration and invasion. Our findings suggest that levels of SAG and COPB2 expression may be useful prognostic indicators in breast cancers and that SAG may be involved in COPB2-related signaling during breast cancer development.
Highlights
Cardiac fibrosis (CF) is characterized by increased activity of cardiac fibroblasts and the production of excessive extracellular matrix (ECM) in the myocardium [1]
Www.aging-us.com or miR-543 mimics followed by real-time PCR to detect lnc lncRNA Homo sapiens ring finger protein 7 (RNF7) and THBS1 associated with Argonaute 2 (AGO2); the results shown in Figure 6G confirmed the interaction between lnc RNF7 and miR-543, and between THBS1 and miR-543
Microarray profiling analysis revealed that a total of 294 mRNAs and 107 long noncoding RNAs (lncRNAs) were differentially-expressed in CF rat hearts
Summary
Cardiac fibrosis (CF) is characterized by increased activity of cardiac fibroblasts and the production of excessive extracellular matrix (ECM) in the myocardium [1]. TGFβ1 induces myofibroblast transdifferentiation and enhances ECM protein expression [9, 10]. The matricellular protein Thrombospondin 1 (TSP1) is a physiologic regulator of latent TGFβ activation in vitro and in many homeostatic and pathologic conditions in vivo [12,13,14,15]. The increases in TSP1 expression result in enhanced TGFβ activation and increased synthesis of ECM proteins. These data suggest that TSP1 plays a vital role in the development of fibrosis via enhancing TGFβ activation
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