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Antisense oligonucleotides directed against insulin-like growth factor-II messenger ribonucleic acids delay the

Miltu Kumar Ghosh1, Falguni Patra2, Shampa Ghosh2

  • 1Department of Pharmaceutical Technology, Jadavpur University, Kolkata, West Bengal, India ; Georg-August-Universität Göttingen, Department of Human Genetics, Heinrich-Düker Weg 12, 37073 Göttingen, Germany.

Journal of Carcinogenesis
|April 17, 2014
PubMed
Abstract

Insights

Antisense oligonucleotides (ASOs) targeting insulin-like growth factor-II (IGF-II) messenger RNA significantly reduced liver cancer development in a rat model. Two ASO types effectively controlled IGF-II overexpression, delaying hepatic cancer progression.

Area of Science:

  • Oncology
  • Molecular Biology
  • Hepatology

Background:

  • Hepatocellular carcinoma (HCC) is a complex cancer driven by genetic alterations.
  • Insulin-like growth factor-II (IGF-II) is implicated in HCC development and progression.
  • IGF-II is a mitogenic polypeptide found in fetal tissues and expressed in HCC.

Purpose of the Study:

  • To investigate the anticancer potential of phosphorothioate antisense oligonucleotides (ASOs) against IGF-II.
  • To evaluate ASOs targeting coding exons 1, 2, and 3 of IGF-II mRNA.
  • To assess the efficacy in a rat hepatocarcinogenesis model.

Main Methods:

  • Diethylnitrosamine and 2-acetylaminofluorene were used to induce hepatocarcinogenesis in rats.
  • Rats were treated with ASOs targeting IGF-II mRNA.
  • Biochemical and histological analyses were performed to assess treatment effects.

Main Results:

  • 40% of rats treated with ASOs against exon-1 or exon-3 showed no hepatic lesions, nodules, or tumors.
  • Remaining rats exhibited reduced lesion incidence, with 59% and 55% fewer altered foci.
  • ASO treatment led to reduced lesion area, improved hepatocellular integrity, and modulated preneoplastic/neoplastic markers.

Conclusions:

  • Two of three tested ASO types effectively controlled IGF-II overexpression.
  • These ASOs delayed the development and/or progression of hepatic cancer in rats.
  • ASOs represent a potential therapeutic strategy for HCC.
Keywords:
Antisense oligonucleotideshepatic altered focihepatocellular carcinomahyperplastic nodulesinsulin-like growth factor

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