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MYC interaction with the tumor suppressive SWI/SNF complex member INI1 regulates transcription and cellular

Angelina Stojanova1,2, William B Tu1,2, Romina Ponzielli2

  • 1a Department of Medical Biophysics , Faculty of Medicine, University of Toronto , Toronto , Ontario , Canada.

Cell Cycle (Georgetown, Tex.)
|June 9, 2016
PubMed

Insights

The MYC oncogene and INI1 tumor suppressor have opposing roles in gene regulation and cell growth. Re-expressing INI1 suppresses MYC-driven cancer cell proliferation and transformation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • MYC is a crucial oncogene driving cellular transformation and is frequently deregulated in human cancers.
  • INI1 (SMARCB1) is a tumor suppressor and core component of the SWI/SNF chromatin remodeling complex, inactivated in malignant rhabdoid tumors.
  • The precise molecular and functional interplay between MYC and INI1 remains incompletely understood.

Purpose of the Study:

  • To elucidate the molecular interaction between MYC and INI1.
  • To investigate the functional consequences of the MYC-INI1 interaction in cancer, particularly in INI1-deficient contexts.
  • To define the antagonistic roles of MYC and INI1 in cellular and oncogenic functions.

Main Methods:

  • Characterization of MYC-INI1 protein-protein interactions and mapping of binding domains in mammalian cells.
  • Protein-protein interaction network analysis to contextualize MYC-INI1 within chromatin regulatory complexes.
  • Genome-wide analysis of DNA-binding regions and target genes for MYC and INI1.
  • Functional studies in an INI1-deficient rhabdoid tumor model with INI1 re-expression.

Main Results:

  • The minimal binding domains for MYC and INI1 interaction were mapped to functionally relevant regions, without disrupting MYC-MAX interaction.
  • MYC and INI1 share significant overlap in DNA-binding regions and target genes, indicating coordinated or opposing regulatory roles.
  • Re-expression of INI1 in INI1-deficient rhabdoid tumors led to MYC and INI1 binding common target genes with opposing effects on gene expression.
  • INI1 re-expression functionally suppressed cell proliferation and MYC-driven transformation.

Conclusions:

  • MYC and INI1 engage in a direct molecular interaction with distinct binding domains.
  • MYC and INI1 exhibit antagonistic transcriptional and functional roles in cellular processes and oncogenesis.
  • INI1 acts as a tumor suppressor by counteracting MYC's oncogenic activities, offering potential therapeutic insights.
Keywords:
INI1/SMARCB1/hSNF5/BAF47MAXSWI/SNF complex/BAF complexc-MYCcellular transformationchromatin regulatory complexprotein-protein interactionrhabdoid tumorstranscriptional regulation

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