Angiogenin as a molecular target for the Treatment of Prostate Cancer

Shuping Li, Soichiro Ibaragi, Guo Fu Hu

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Angiogenin (ANG), a 14 kDa angiogenic ribonuclease, is upregulated in human prostate cancers, especially in hormone refractory diseases, and is the highest upregulated gene in Akt-driven prostate intraepithelial neoplasia (PIN) in mice. ANG has been shown to undergo nuclear translocation in both prostate cancer cells and cancer-associated endothelial cells where it binds to the promoter region of ribosomal DNA (rDNA) and stimulates ribosomal RNA (rRNA) transcription. ANG thus plays an essential role in prostate cancer progression by stimulating both cancer cell proliferation and tumor angiogenesis. A variety of ANG antagonists, including its antisense oligonucleotide, siRNA, soluble binding proteins, monoclonal antibody, enzymatic inhibitors, and nuclear translocation blockers, have all been shown to inhibit prostate cancer in various animal models. Accumulating evidence indicates that ANG is a molecular target for prostate cancer drug development.

Original languageEnglish
Pages (from-to)83-90
Number of pages8
JournalCurrent Cancer Therapy Reviews
Volume7
Issue number2
Publication statusPublished - May 2011
Externally publishedYes

Fingerprint

Prostatic Neoplasms
Neoplasms
Antisense Oligonucleotides
Ribonucleases
Ribosomal DNA
Genetic Promoter Regions
Small Interfering RNA
Prostate
Carrier Proteins
Endothelial Cells
Animal Models
Monoclonal Antibodies
Cell Proliferation
angiogenin
Hormones
Pharmaceutical Preparations
Genes

Keywords

  • Androgen-independence
  • Angiogenesis
  • Angiogenin
  • Prostate cancer
  • rRNA transcription

ASJC Scopus subject areas

  • Oncology
  • Cancer Research
  • Molecular Medicine

Cite this

Angiogenin as a molecular target for the Treatment of Prostate Cancer. / Li, Shuping; Ibaragi, Soichiro; Hu, Guo Fu.

In: Current Cancer Therapy Reviews, Vol. 7, No. 2, 05.2011, p. 83-90.

Research output: Contribution to journalArticle

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