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Papers In Press, published online ahead of print November 21, 2001
Cell Biology, University of Cincinnati, Cincinnati, Ohio 45267
Corresponding Author: shobecm{at}email.uc.edu
The BRG-1 subunit of the SWI/SNF complex is involved in chromatin remodeling and has been implicated the action of the retinoblastoma tumor suppressor (RB). Given the importance of BRG-1 in RB function, germ line BRG-1 mutations in tumorigenesis may be tantamount to RB inactivation. Therefore, in this study we assessed the behavior of cells harboring discrete BRG-1 alleles for the RB signaling pathway. Using p16ink4a, an upstream activator of endogenous RB, or a constitutively active RB construct (PSM-RB) we determined that the majority of tumor lines with germ line defects in BRG-1 were sensitive to RB-mediated cell cycle arrest. By contrast, A427 (lung carcinoma) cells were resistant to expression of p16ink4a and PSM-RB. Analysis of the SWI/SNF subunits in the different tumor lines revealed that A427 are deficient for BRG-1 and its homologue Brm, whereas RB-sensitive cell lines retained Brm expression. Similarly, the RB-resistant SW13 and C33A cell line were also deficient for both BRG-1/Brm. Reintroduction of either BRG-1 or Brm into A427 or C33A cells restored RB-mediated signaling to Cyclin A to cause cell cycle arrest. Consistent with this compensatory role, we observed that Brm could also drive expression of CD44. We also determined that loss of these core SWI/SNF subunits renders SW13 cells resistant to activation of the RB pathway by the chemotherapeutic agent cisplatin (CDDP), since reintroduction of either BRG-1 or Brm into SW13 cells restored the CDDP DNA-damage checkpoint. Together, these data demonstrate that Brm can compensate for BRG-1 loss, as pertains to RB sensitivity.
J. Biol. Chem, 10.1074/jbc.M109532200
Submitted on October 2, 2001
Revised on November 21, 2001
Accepted on November 20, 2001
Compensation of BRG-1 function by Brm: Insight into the role of the core SWI/SNF subunits in RB-signaling
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