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KSHV-encoded miRNAs target MAF to induce endothelial cell reprogramming.

Amy Hansen1, Stephen Henderson, Dimitrios Lagos

  • 1Cancer Research UK Viral Oncology Group, University College London Cancer Institute, University College London, London WC1E 6BT, United Kingdom.

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Kaposi sarcoma herpesvirus (KSHV) microRNAs reprogram infected cells by silencing MAF. This promotes poorly differentiated endothelial cells, contributing to Kaposi sarcoma development.

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Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Kaposi sarcoma herpesvirus (KSHV) alters endothelial cell gene expression.
  • KSHV-infected lymphatic endothelial cells (LECs) express blood vessel endothelial cell (BEC) markers, leading to poorly differentiated tumor cells.
  • MicroRNAs (miRNAs) are key regulators of gene expression.

Purpose of the Study:

  • To validate KSHV-miRNA expression in Kaposi sarcoma lesions.
  • To investigate the role of KSHV-miRNAs in cellular reprogramming.
  • To identify the cellular targets of KSHV-miRNAs involved in oncogenesis.

Main Methods:

  • Expression analysis of KSHV-miRNAs in Kaposi sarcoma lesions.
  • Silencing of the transcription factor MAF by KSHV-miRNAs.
  • Functional studies on MAF's role in maintaining LEC differentiation.

Main Results:

  • KSHV-encoded miRNAs are expressed in Kaposi sarcoma lesions.
  • KSHV-miRNAs silence the transcription factor MAF.
  • MAF acts as a repressor of BEC-specific genes, maintaining LEC differentiation.

Conclusions:

  • KSHV-miRNAs contribute to viral-induced reprogramming by targeting MAF.
  • MAF's repression of BEC genes is crucial for LEC differentiation.
  • Viral miRNAs can alter host cell differentiation, promoting KSHV oncogenesis.