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A Multifunctional LNA Oligonucleotide-Based Strategy Blocks AR Expression and Transactivation Activity in PCa Cells.

Daniela Castanotto1, Xiaowei Zhang1, Jacqueline Rüger1

  • 1Department of Medical Oncology, City of Hope, 1500 East Duarte Road, Duarte, CA 91010, USA.

Molecular Therapy. Nucleic Acids
|December 18, 2020
PubMed
Summary
This summary is machine-generated.

New splice-switching oligonucleotides (SSOs) target the androgen receptor (AR) in prostate cancer (PCa). These SSOs block AR

Keywords:
AR45ARV7ASONMDONPSTSSOnonsense codonsplicing

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • The androgen receptor (AR) is crucial for prostate cancer (PCa) progression by activating androgen-induced genes.
  • Inhibiting AR-mediated transcription is a key strategy to control PCa growth and metastasis.

Purpose of the Study:

  • To develop novel therapeutic molecules targeting the androgen receptor (AR) for prostate cancer (PCa) treatment.
  • To investigate the potential of splice-switching oligonucleotides (SSOs) to modulate AR splicing and function.

Main Methods:

  • Utilized tailor-made splice-switching locked nucleic acid (LNA) oligonucleotides (SSOs) to alter AR precursor mRNA splicing.
  • Introduced premature stop codons to destabilize AR transcripts and favored the production of the AR45 isoform.
  • Screened SSOs for dual function: silencing full-length AR and promoting the inhibitory AR45 isoform.

Main Results:

  • SSOs successfully redirected AR pre-mRNA splicing, leading to transcript destabilization and reduced full-length AR.
  • Selected SSOs promoted the expression of AR45, an AR isoform that antagonizes AR activity.
  • The developed SSOs effectively silenced AR expression and modulated AR-responsive genes.

Conclusions:

  • A bi-functional SSO strategy offers a novel therapeutic approach for prostate cancer (PCa) by targeting AR.
  • This approach simultaneously silences AR and promotes an inhibitory AR isoform (AR45).
  • The strategy is potentially adaptable for other therapies requiring gene silencing and isoform modulation.