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A nuclear NKRF interacting long noncoding RNA controls EBV eradication and suppresses tumor progression in natural

Wen-Fang Wang1, Hui-Juan Zhong2, Shu Cheng2

  • 1Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China; School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.

Biochimica Et Biophysica Acta. Molecular Basis of Disease
|April 21, 2023
PubMed

Insights

Long intergenic noncoding RNA (lincRNA) LINC00486 suppresses Epstein-Barr virus (EBV)-driven natural killer T cell lymphoma (NKTCL) by inhibiting tumor growth and enhancing viral eradication. This lincRNA targets NKRF to modulate NF-κB signaling and SLC1A1 expression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Virology

Background:

  • Long intergenic noncoding RNAs (lincRNAs) are implicated in tumor progression, but their role in Epstein-Barr virus (EBV)-driven natural killer T cell lymphoma (NKTCL) is not fully understood.
  • Understanding the molecular pathogenesis of lincRNAs in EBV-driven NKTCL is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of lincRNAs in EBV-driven NKTCL.
  • To identify specific lincRNAs involved in NKTCL pathogenesis and elucidate their mechanisms of action.

Main Methods:

  • High-throughput RNA sequencing of 439 lymphoma samples to profile ncRNA expression.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) for validation of LINC00486 downregulation.
  • In vitro and in vivo studies to assess the functional role of LINC00486.
  • Chromatin Immunoprecipitation (ChIP) and luciferase assays to determine molecular interactions and transcriptional regulation.

Main Results:

  • LINC00486 was identified as a significantly downregulated lincRNA in EBV-encoded RNA (EBER)-positive lymphoma, particularly NKTCL.
  • LINC00486 demonstrated tumor suppressive functions by inhibiting cell growth and inducing G0/G1 cell cycle arrest.
  • LINC00486 interacted with NKRF, abrogating its binding to p65, activating NF-κB/TNF-α signaling, and enhancing EBV eradication.
  • NKRF was found to transcriptionally downregulate Solute carrier family 1 member 1 (SLC1A1), a mediator of glutamine addiction and tumor progression in NKTCL.

Conclusions:

  • LINC00486 acts as a tumor suppressor in NKTCL by counteracting EBV infection.
  • The findings enhance the understanding of EBV-driven oncogenesis in NKTCL.
  • Targeting EBV eradication presents a potential clinical strategy for anti-cancer treatment in NKTCL.
Keywords:
EBVLong intergenic noncoding RNAsNF-κBNKRFNatural killer T cell lymphomaSLC1A1

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