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Concomitant down-regulation of BRM and BRG1 in human tumor cell lines: differential effects on RB-mediated growth

David N Reisman1, Matthew W Strobeck, Bryan L Betz

  • 1Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599-7295, USA.

Oncogene
|February 19, 2002
PubMed

Insights

Mammalian cells have two SWI/SNF chromatin-remodeling subunits, BRG1 and BRM. Both are down-regulated in tumors, but BRM can restore cell cycle arrest and CD44 expression, indicating distinct roles.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Mammalian cells utilize SWI/SNF chromatin-remodeling complexes, with two key subunits: BRG1 and BRM.
  • The functional overlap and distinct roles of BRG1- and BRM-containing SWI/SNF complexes are not fully understood.

Purpose of the Study:

  • To investigate the functional relationship between BRG1 and BRM in mammalian cells, particularly in the context of cancer.
  • To determine if BRM can compensate for BRG1 loss in aberrant cellular functions associated with tumors.

Main Methods:

  • Analysis of BRG1 and BRM mRNA levels in human tumor cell lines.
  • Functional assays using transient transfection to assess BRM's effect on cell cycle arrest, CD44, and Cyclin A expression.
  • Examination of CD44 expression in tissues from BRM-null mice.

Main Results:

  • Concomitant down-regulation of BRG1 and BRM mRNA was observed in six human tumor cell lines.
  • BRM expression restored RB-mediated cell cycle arrest, induced CD44 protein, and suppressed Cyclin A expression in tumor cells.
  • BRM-containing SWI/SNF complexes are crucial for CD44 gene regulation under physiological conditions.

Conclusions:

  • BRG1 and BRM share some redundant functions, explaining their co-down-regulation in neoplastic progression.
  • BRM plays a distinct role in regulating CD44 expression, highlighting non-interchangeable functions between BRG1- and BRM-containing SWI/SNF complexes.

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