Role of PRMT1 and PRMT5 in Breast Cancer.

Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE

Original Publication: Basel, Switzerland : MDPI, [2000-

Protein-Arginine N-Methyltransferases*/metabolism ; Protein-Arginine N-Methyltransferases*/genetics ; Breast Neoplasms*/metabolism ; Breast Neoplasms*/genetics ; Breast Neoplasms*/pathology ; Repressor Proteins*/metabolism ; Repressor Proteins*/genetics; Humans ; Female ; Signal Transduction ; Methylation ; Epigenesis, Genetic ; Animals ; Gene Expression Regulation, Neoplastic

Breast cancer is the most common cancer diagnosed in women worldwide. Early-stage breast cancer is curable in ~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.

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00107943 Fondation de France; ARC2022 Fondation Arc

Keywords: PRMT1; PRMT5; arginine methylation; breast cancer; cell signaling; transcriptional regulation

EC 2.1.1.319 (Protein-Arginine N-Methyltransferases)
EC 2.1.1.319 (PRMT1 protein, human)
0 (Repressor Proteins)
EC 2.1.1.319 (PRMT5 protein, human)

Date Created: 20240829 Date Completed: 20240829 Latest Revision: 20240903

20240903

PMC11354362

10.3390/ijms25168854

39201539