MYBL2 amplification in breast cancer: Molecular mechanisms and therapeutic potential

Research output: Contribution to journalReview articlepeer-review

Abstract

The MYBL2 gene, also known as B-MYB, is essential to regulate vital cellular processes including cell proliferation, differentiation and DNA repair. Changes in these pathways can facilitate cancer development and as such targeting these processes represent an effective method to treat multiple cancer types. Alterations in gene expression have been identified in cancer cells including changes in MYBL2, which appears to be of particular significance in breast cancer (BC) patients. Upregulation of MYBL2 in BC can occur via multiple mechanisms, including changes in regulation by micro RNAs, amplification of the 20q13 gene coding region and single nucleotide polymorphisms in the MYBL2 gene itself or associated genes. Evidence from multiple studies suggests MYBL2 expression could be used as a biomarker for disease severity in BC patients, which could identify those who require a more targeted treatment approach to prevent disease recurrence. In fact, high MYBL2 expression correlates with BC metastasis, worse relapse free survival and shorter overall survival, providing strong evidence that upregulation of MYBL2 functions contributes to more aggressive disease. This review summarises the significance of amplified MYBL2 expression to the development and pathogenesis of BC and suggests ways to target this multifunctional protein as an effective treatment to prevent disease recurrence.

Original languageEnglish
Pages (from-to)188407
JournalBiochimica et Biophysica Acta - Reviews on Cancer
Volume1874
Issue number2
DOIs
Publication statusPublished - Dec 2020

Bibliographical note

Copyright © 2020 Elsevier B.V. All rights reserved.

Keywords

  • Biomarkers, Tumor/genetics
  • Breast Neoplasms/genetics
  • Cell Cycle Proteins/genetics
  • Female
  • Gene Amplification
  • Gene Expression Regulation
  • Humans
  • Polymorphism, Single Nucleotide
  • Prognosis
  • Survival Analysis
  • Trans-Activators/genetics
  • Up-Regulation

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