BAF180 is a critical regulator of p21 induction and a tumor suppressor mutated in breast cancer

Wei Xia, Satoru Nagase, Amy Gerstein Montia, Sergey M. Kalachikov, Megan Keniry, Tao Su, Lorenzo Memeo, Hanina Hibshoosh, Ramon Parsons

Research output: Contribution to journalArticlepeer-review

121 Citations (Scopus)

Abstract

Screening for tumor suppressor genes in breast cancer revealed multiple truncating mutations of PB1, which encodes the BAF180 subunit of the PBAF chromatin remodeling complex. Mutation was associated with loss of heterozygosity of the wild-type allele. BAF180 complementation of BAF180-mutant tumor cells caused G1 arrest that was dependent on increased expression of the cyclin/cyclin-dependent kinase inhibitor p21/WAF1/CIP1. Endogenous wild-type BAF180 bound to the p21 promoter and was required for proper p21 expression and G1 arrest after transforming growth factor-β and γ-radiation treatment. BAF180 thus functions on two tumor suppressor signaling pathways as a physiologic mediator of p21 expression. We conclude that BAF180 suppresses tumorigenesis, at least in part, through its ability to regulate p21.

Original languageEnglish
Pages (from-to)1667-1674
Number of pages8
JournalCancer Research
Volume68
Issue number6
DOIs
Publication statusPublished - 2008 Mar 15
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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