scholarly journals Alternatively spliced protein arginine methyltransferase 1 isoform PRMT1v2 promotes the survival and invasiveness of breast cancer cells

Cell Cycle ◽  
2012 ◽  
Vol 11 (24) ◽  
pp. 4597-4612 ◽  
Author(s):  
R. Mitchell Baldwin ◽  
Alan Morettin ◽  
Genevieve Paris ◽  
Isabelle Goulet ◽  
Jocelyn Côté
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Protein Arginine Methyltransferase ◽  
Arginine Methyltransferase ◽  
Alternatively Spliced ◽  
Protein Arginine Methyltransferase 1 ◽  
Methyltransferase 1

scholarly journals Cytoplasmic sequestration of FUS/TLS associated with ALS alters histone marks through loss of nuclear protein arginine methyltransferase 1

2014 ◽  
Vol 24 (3) ◽  
pp. 773-786 ◽  
Author(s):  
Michael Tibshirani ◽  
Miranda L. Tradewell ◽  
Katie R. Mattina ◽  
Sandra Minotti ◽  
Wencheng Yang ◽  
...  
Keyword(s):  
Nuclear Protein ◽  
Protein Arginine Methyltransferase ◽  
Arginine Methyltransferase ◽  
Histone Marks ◽  
Protein Arginine Methyltransferase 1 ◽  
Methyltransferase 1

Abstract 457: Protein Arginine Methyltransferase-1 is Required for Epicardial Epithelial-to-Mesenchymal Transition

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Olan Jackson-Weaver ◽  
Jian Wu ◽  
Yongchao Gou ◽  
Shihong Shi ◽  
Henry Sucov ◽  
...  
Keyword(s):  
Cell Types ◽  
Protein Arginine Methyltransferase ◽  
Arginine Methyltransferase ◽  
P53 Expression ◽  
Epicardial Cells ◽  
Epicardial Cell ◽  
Protein Arginine Methyltransferase 1 ◽  
E Cadherin ◽  
Methyltransferase 1

Rationale: Epicardial epithelial-to-mesenchymal trasition (EMT) is a vital process in embryonic heart development. During EMT, epicardial cells acquire migratory and invasive properties, and differentiate into new cell types, including cardiac fibroblasts and coronary smooth muscle cells. EMT is characterized by an increase in mesenchymal proteins such as Slug and Fibronectin, and a decrease in cell-junction proteins such as E-Cadherin, and is dependent on TGF-β signaling. We have recently demonstrated that protein arginine methyltransferase-1 (PRMT1) is necessary for TGF-β family signaling and EMT in non-epicardial cell types. Objective: To determine the role of PRMT1 in epicardial EMT. Methods and Results: We investigated the role of PRMT1 in epicardial EMT in mouse epicardial cells. PRMT1 siRNA prevented the increase in Slug and Fibronectin and the decrease in E-Cadherin in TGF-β treatment-induced EMT of mouse epicardial cell line MEC1. PRMT1 siRNA also reduced the migration and invasion of MEC1 cells. These results demonstrate that PRMT1 is required for epicardial EMT. In WT1-Cre ERT ;ROSA-YFP fl/fl mouse embryos, PRMT1 siRNA reduced epicardial EMT in a thorax culture model. Among the key transcription factors that regulate the EMT program, Slug, but not Snail, is specifically regulated by PRMT1. We further identified that PRMT1 siRNA also increased the expression of p53, a key regulator of the Slug degradation pathway. PRMT1 siRNA increases p53 expression by decreasing p53 degradation, and shifted p53 localization to the cytoplasm. In vitro methylation assays further demonstrated that PRMT1 methylates p53. Knockdown of p53 increased Slug levels and enhanced EMT, establishing p53 as a regulator of epicardial EMT through controlling Slug expression. Conclusions: The PRMT1-p53-Slug pathway is necessary for epicardial EMT in cultured MEC1 cells as well as in the epicardium ex vivo .

Sign in / Sign up

Export Citation Format

Share Document