2. Academic Validation
  3. EIF4A3 is stabilized by the long noncoding RNA BC200 to regulate gene expression during Epstein-Barr virus infection

EIF4A3 is stabilized by the long noncoding RNA BC200 to regulate gene expression during Epstein-Barr virus infection

  • J Med Virol. 2024 Oct;96(10):e29955. doi: 10.1002/jmv.29955.
Jing Li 1 2 3 4,  Yujie Xin 1 2 3 4,  Siwei Zhang 1 2 3 5,  Yanling Li 1 2,  Mingjuan Jiang 1 2 3 4,  Senmiao Zhang 1 2 3 4,  Li Yang 1 2 3 4,  Jing Yang 1 2 3,  Pengfei Cao 3 4,  Jianhong Lu 1 2 3 4
Affiliations

Affiliations

  • 1 Department of Nuclear Medicine, Hunan Cancer Hospital/the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, China.
  • 2 Department of Microbiology, School of Basic Medical Science, Central South University, Changsha, China.
  • 3 The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, NHC Key Laboratory of Carcinogenesis, Cancer Research Institute, Central South University, Changsha, China.
  • 4 Department of Hematology, Xiangya Hospital, Central South University, Changsha, China.
  • 5 Laboratory Medicine Center, Zhuzhou Central Hospital/The Affiliated Zhuzhou Hospital of Xiangya School of Medicine, Central South University, Zhuzhou, China.
PMID: 39370864 DOI: 10.1002/jmv.29955
Abstract

Epstein‒Barr virus (EBV) regulates the expression of host genes involved in functional pathways for viral Infection and pathogenicity. Long noncoding RNAs (lncRNAs) have been found to be important regulators of cellular biology. However, how EBV affects host biological processes via lncRNAs remains elusive. Eukaryotic initiation factor 4A3 (EIF4A3) was recently identified as an essential controller of cell fate with an unknown role in EBV Infection. Here, the expression of lncRNA brain cytoplasmic 200 (BC200) was shown to be significantly upregulated in EBV-infected cell lines. RNA immunoprecipitation and RNA pulldown assays confirmed that BC200 bound to EIF4A3. Moreover, BC200 promoted EIF4A3 expression at the protein level but not at the mRNA level. Mechanistically, BC200 stabilized the EIF4A3 protein by impeding the K48-linked polyubiquitination of the K195 and K198 residues of EIF4A3. In addition, RNA-seq analysis of EBV-positive cells with knockdown of either BC200 or EIF4A3 revealed that a broad range of cellular genes were differentially regulated, particularly those related to virus Infection and immune response pathways. This study is the first to reveal the key residues involved in EIF4A3 polyubiquitination and elucidate the novel regulatory role of EBV in host gene expression via the BC200/EIF4A3 axis. These results have implications for the pathogenesis and treatment of EBV-related diseases.

Keywords

EIF4A3; Epstein–Barr virus; gene expression; long noncoding RNA; ubiquitination.

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