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The potential of targeting Sin3B and its associated complexes for cancer therapy

David J Cantor1, Gregory David1,2,3

  • 1a Department of Biochemistry and Molecular Pharmacology , New York University School of Medicine , New York , NY , USA.

Expert Opinion on Therapeutic Targets
|September 29, 2017
PubMed
Abstract

Insights

Sin3B protein complexes are crucial for controlling gene activity and cell cycles. Inhibiting these complexes may offer new cancer treatment strategies by targeting tumor progression and therapy resistance.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Biology

Background:

  • Sin3B acts as a scaffold for chromatin-modifying complexes that repress gene transcription.
  • Sin3B-containing complexes are essential for cell cycle withdrawal, impacting tumor progression.
  • Dysregulation of Sin3B-dependent cell cycle exit contributes to cancer development.

Purpose of the Study:

  • To review the biochemical characteristics of Sin3B-containing complexes.
  • To explore the mechanisms by which these complexes regulate gene transcription.
  • To discuss the role of Sin3B in conjunction with Rb family proteins in repressing E2F target genes during key cellular processes.

Main Methods:

  • Literature review of Sin3B-containing complexes.
  • Analysis of Sin3B's role in gene transcription regulation.
  • Examination of Sin3B's association with Rb proteins and E2F target genes.

Main Results:

  • Sin3B complexes regulate gene transcription through chromatin modification.
  • Sin3B-dependent cell cycle exit is critical for normal biological processes.
  • Association with Rb proteins mediates repression of E2F target genes in quiescence, differentiation, and senescence.

Conclusions:

  • Sin3B-containing complexes are key regulators of cell cycle and gene expression.
  • Targeting Sin3B complexes presents a potential therapeutic strategy for cancer treatment.
  • Further characterization of Sin3B complexes can help overcome cancer stem cell resistance and SASP-related tumor promotion.
Keywords:
Cancer stem cellSin3Bcellular senescencechromatin modifiersquiescencesenescence associated secretory phenotype

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