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Suppression of activin-induced apoptosis by novel antisense strategy in human prostate cancer cells

S Y Ying1, C M Chuong, S Lin

  • 1Department of Cell and Neurobiology, University of Southern California, School of Medicine, BMT-401, 1333 San Pablo Street, Los Angeles, California, 90033, USA. sying@hsc.usc.edu

Biochemical and Biophysical Research Communications
|December 22, 1999
PubMed

Insights

Apoptosin, a protein crucial for prostate cancer cell death, was targeted using antisense probes. Blocking apoptosin prevented cancer cell apoptosis, highlighting its role in regulating cell death.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Apoptosin is a novel gene encoding a protein with a mitotic kinase-motif.
  • Activin, part of the TGF-beta family, stimulates apoptosin in prostate cancer cells and tissues.

Purpose of the Study:

  • To investigate the role of apoptosin in the regulation of apoptosis in human prostate cancer.
  • To explore the potential of targeting apoptosin for therapeutic intervention in prostate cancer.

Main Methods:

  • Utilized gene knockout methodology involving chemically modified antisense probes targeting apoptosin mRNA.
  • Employed covalent bonding of antisense probes to mRNA to prevent translation and post-transcriptional modification.
  • Assessed the impact of antisense apoptosin introduction on activin-induced apoptosis in LNCaP cells.

Main Results:

  • Antisense probes successfully inhibited apoptosin mRNA translation, leading to no protein synthesis.
  • Introduction of antisense apoptosin prevented apoptosis in cancer cells.
  • Apoptosin inhibition interfered with genomic DNA fragmentation and released cell cycle checkpoints.

Conclusions:

  • Apoptosin plays a significant role in the apoptotic regulation of human prostate cancer.
  • Apoptosin, alongside p53, is a key factor in controlling cell death in prostate cancer.
  • Targeting apoptosin presents a potential strategy for managing prostate cancer.

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