Role of PRMT1 and PRMT5 in Breast Cancer

被引:2
|
作者
Martinez, Sebastien [1 ,2 ]
Sentis, Stephanie [1 ,2 ]
Poulard, Coralie [1 ,2 ]
Tredan, Olivier [1 ,2 ,3 ]
Le Romancer, Muriel [1 ,2 ]
机构
[1] Univ Claude Bernard Lyon 1, Ctr Rech Cancerol Lyon, Inserm, U1052, F-69000 Lyon, France
[2] Univ Claude Bernard Lyon 1, Ctr Rech Cancerol Lyon, CNRS,UMR5286, F-69000 Lyon, France
[3] Ctr Leon Berard, Oncol Dept, F-69008 Lyon, France
关键词
PRMT1; PRMT5; arginine methylation; breast cancer; transcriptional regulation; cell signaling; REGULATORY T-CELLS; ARGININE METHYLATION; DNA-REPAIR; HOMOLOGOUS RECOMBINATION; PARP INHIBITION; MESSENGER-RNA; SM PROTEINS; C/EBP-ALPHA; GAR MOTIF; IN-VIVO;
D O I
10.3390/ijms25168854
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Breast cancer is the most common cancer diagnosed in women worldwide. Early-stage breast cancer is curable in similar to 70-80% of patients, while advanced metastatic breast cancer is considered incurable with current therapies. Breast cancer is a highly heterogeneous disease categorized into three main subtypes based on key markers orientating specific treatment strategies for each subtype. The complexity of breast carcinogenesis is often associated with epigenetic modification regulating different signaling pathways, involved in breast tumor initiation and progression, particularly by the methylation of arginine residues. Protein arginine methyltransferases (PRMT1-9) have emerged, through their ability to methylate histones and non-histone substrates, as essential regulators of cancers. Here, we present an updated overview of the mechanisms by which PRMT1 and PRMT5, two major members of the PRMT family, control important signaling pathways impacting breast tumorigenesis, highlighting them as putative therapeutic targets.
引用
收藏
页数:25
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