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Remodeling oncogenic transcriptomes by small molecules targeting NONO.

Stefan G Kathman1, Seong Joo Koo2, Garrett L Lindsey3

  • 1Department of Chemistry, The Scripps Research Institute, La Jolla, CA, USA. skathman@scripps.edu.

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|March 2, 2023
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Summary
This summary is machine-generated.

Researchers developed small molecule probes targeting the RNA-binding protein NONO (nodal vesicular nucleon associated protein). These probes suppress cancer-driving genes and impair prostate cancer cell growth by trapping NONO.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Chemical Biology

Background:

  • The human proteome extensively participates in messenger RNA (mRNA) homeostasis.
  • A significant gap exists in chemical probes for most RNA-binding proteins (RBPs).

Purpose of the Study:

  • To identify chemical probes targeting RBPs involved in mRNA homeostasis.
  • To investigate the therapeutic potential of targeting the androgen receptor (AR) pathway in prostate cancer.

Main Methods:

  • Development of electrophilic small molecules.
  • Chemical proteomics for target engagement identification.
  • Gene expression analysis (transcriptomics).
  • Cell proliferation assays.
  • Genetic manipulation (gene knockout and rescue experiments).

Main Results:

  • Identified small molecules that decrease androgen receptor (AR) and its splice variants' transcript expression in prostate cancer cells.
  • Demonstrated covalent engagement of the RNA-binding protein NONO (nodal vesicular nucleon associated protein) at Cysteine 145 (C145).
  • Showed that covalent NONO ligands suppress numerous cancer-relevant genes and inhibit cancer cell proliferation.
  • Established that NONO knockout cells are resistant to these ligands, with sensitivity restored by wild-type NONO reintroduction.
  • Revealed that ligands promote NONO nuclear foci accumulation and stabilize NONO-RNA interactions, suggesting a trapping mechanism.

Conclusions:

  • NONO can be targeted by covalent small molecules to suppress protumorigenic transcriptional networks.
  • The identified NONO ligands offer a potential therapeutic strategy for cancers driven by AR signaling.
  • The mechanism involves NONO trapping, potentially preventing compensation by paralog proteins like PSPC1 and SFPQ.