EBV miR-BARTs and human lncRNAs: Shifting the balance in competing endogenous RNA networks in EBV-associated gastric cancer

Biochim Biophys Acta Mol Basis Dis. 2021 Apr 1;1867(4):166049. doi: 10.1016/j.bbadis.2020.166049. Epub 2021 Jan 2.

Abstract

Non-coding RNAs (ncRNAs) contribute to the regulation of gene expression. By acting as competing endogenous RNA (ceRNA), long non-coding RNAs (lncRNAs) hijack microRNAs (miRNAs) and inhibit their ability to bind their coding targets. Viral miRNAs can compete with and target the same transcripts as human miRNAs, shifting the balance in networks associated with multiple cellular processes and diseases. Epstein-Barr virus (EBV) is an example of how a subset of viral coding RNA and non-coding RNAs can cause deregulation of human transcripts and contribute to the development of EBV-associated malignancies. EBV non-coding transforming genes include lncRNAs (i.e circular RNAs), and small ncRNAs (i.e. miRNAs). Among the latter, most ongoing research has focused on miR-BARTs whereas target many genes associated with apoptosis and epithelial-mesenchymal transition, in EBV-associated gastric cancer (GC). In this review, we propose to include the interactions between EBV ncRNAs human transcripts in the hypothesis known as "competitive viral and host RNAs". These interactions may shift the balance in biological pathways such as apoptosis and epithelial-mesenchymal transition in EBV-associated gastric cancer.

Keywords: Apoptosis; Competitive viral and host RNAs; EBV-associated gastric cancer; Epithelial to mesenchymal transition; Long non-coding; miR-BARTs.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Epithelial-Mesenchymal Transition
  • Epstein-Barr Virus Infections / complications
  • Epstein-Barr Virus Infections / genetics*
  • Epstein-Barr Virus Infections / virology
  • Gene Expression Regulation, Neoplastic
  • Gene Regulatory Networks
  • Herpesvirus 4, Human / genetics*
  • Herpesvirus 4, Human / physiology
  • Host-Pathogen Interactions
  • Humans
  • MicroRNAs / genetics*
  • RNA, Long Noncoding / genetics*
  • RNA, Viral / genetics*
  • Stomach Neoplasms / etiology
  • Stomach Neoplasms / genetics*
  • Stomach Neoplasms / virology

Substances

  • MicroRNAs
  • RNA, Long Noncoding
  • RNA, Viral