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An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus
09:53

An In Vitro Model for Studying Cellular Transformation by Kaposi Sarcoma Herpesvirus

Published on: August 25, 2017

Inhibition of Kaposi's sarcoma in vivo by fenretinide

Nicoletta Ferrari1, Monica Morini, Ulrich Pfeffer

  • 1Molecular Oncology Laboratory, the National Institute for Cancer Research, Genova, Italy.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|December 17, 2003
PubMed
Abstract

Insights

Fenretinide (4HPR) effectively inhibits Kaposi

Area of Science:

  • Oncology
  • Molecular Biology
  • Angiogenesis Research

Background:

  • Kaposi's sarcoma (KS) is a highly angiogenic malignancy often associated with immune suppression.
  • Current therapies for KS, including highly active antiretroviral therapy (HAART), carry risks of recurrence.
  • Novel therapeutic strategies targeting tumor growth and angiogenesis are needed for KS management.

Purpose of the Study:

  • To evaluate the efficacy of fenretinide [N-(4-hydroxyphenyl)retinamide; (4HPR)] against highly angiogenic Kaposi's sarcoma (KS) tumors in vivo.
  • To elucidate the underlying mechanisms of 4HPR's action on KS tumor growth and angiogenesis.
  • To explore the potential clinical applications of 4HPR as a chemopreventive or therapeutic agent for KS.

Main Methods:

  • Tumor xenograft models using KS-Imm cells in nude mice were treated with 4HPR or vehicle.
  • In vitro studies assessed 4HPR's effects on KS-Imm and endothelial cell proliferation, apoptosis, migration, and invasion.
  • In vivo angiogenesis was evaluated using a Matrigel plug assay, with examination of angiogenesis-related molecules and retinoid receptors at mRNA and protein levels.

Main Results:

  • 4HPR significantly reduced the growth of Kaposi's sarcoma xenografts in vivo and inhibited angiogenesis in the Matrigel assay.
  • In vitro, 4HPR impacted KS-Imm and endothelial cell growth, migration, and invasion, notably decreasing matrix metalloprotease-2 activity.
  • 4HPR treatment led to reduced vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor 2 (VEGFR2) expression, and increased retinoic acid receptor beta expression.

Conclusions:

  • Fenretinide (4HPR) demonstrates significant in vivo efficacy against Kaposi's sarcoma by inhibiting tumor growth and angiogenesis.
  • The mechanism involves modulating angiogenesis factors (VEGF, VEGFR2) and their receptors, and inhibiting invasion via matrix metalloprotease-2.
  • These findings support further investigation of 4HPR as a potential chemopreventive or therapeutic agent for Kaposi's sarcoma.

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