Propranolol Decreases Proliferation of Endothelial Cells Transformed by Kaposi's Sarcoma-Associated Herpesvirus and Induces Lytic Viral Gene Expression

J Virol. 2015 Nov;89(21):11144-9. doi: 10.1128/JVI.01569-15. Epub 2015 Aug 12.

Abstract

Kaposi's sarcoma (KS) is common in Africa, but economic constraints hinder successful treatment in most patients. Propranolol, a generic β-adrenergic antagonist, decreased proliferation of KS-associated herpesvirus (KSHV)-infected cells. Downregulation of cyclin A2 and cyclin-dependent kinase 1 (CDK1) recapitulated this phenotype. Additionally, propranolol induced lytic gene expression in association with downregulation of CDK6. Thus, propranolol has diverse effects on KSHV-infected cells, and this generic drug has potential as a therapeutic agent for KS.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adrenergic beta-Antagonists / pharmacology*
  • CDC2 Protein Kinase
  • Cell Proliferation / drug effects*
  • Cyclin A2 / metabolism
  • Cyclin-Dependent Kinases / metabolism
  • Endothelial Cells / drug effects
  • Endothelial Cells / virology*
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Herpesvirus 8, Human / metabolism*
  • Humans
  • Propranolol / pharmacology*
  • Sarcoma, Kaposi / drug therapy*

Substances

  • Adrenergic beta-Antagonists
  • CCNA2 protein, human
  • Cyclin A2
  • Propranolol
  • CDC2 Protein Kinase
  • CDK1 protein, human
  • Cyclin-Dependent Kinases