ARID1A and CEBPα cooperatively inhibit UCA1 transcription in breast cancer

Xiao Guo, Yin Zhang, Anand Mayakonda, Vikas Madan, Ling Wen Ding, Le Hang Lin, Saadiya Zia, Sigal Gery, Jeffrey W. Tyner, Wu Zhou, Dong Yin, De Chen Lin, H. Phillip Koeffler

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


As one of the primary members of SWI/SNF chromatin remodeling complexes, ARID1A contains frequent loss-of-function mutations in many types of cancers. However, the molecular mechanisms underlying ARID1A deficiency in cancer biology remain to be investigated. Using breast cancer as a model, we report that silencing ARID1A significantly increased cellular proliferation and migration. Mechanistically, primarily functioning as a transcriptional repressor, loss of ARID1A profoundly alters histone modifications and the transcriptome. Notably, ARID1A inhibited the expression of a long non-coding RNA, UCA1, by regulating chromatin access of the transcription factor CEBPα. Restoration experiments showed that UCA1 mediates the functions of ARID1A that induces loss of cellular proliferation and migration. Together, our findings characterize ARID1A as a key tumor-suppressor gene in breast cancer through cooperation with CEBPα, and loss-of-function mutations of ARID1A activates UCA1.

Original languageEnglish (US)
Pages (from-to)5939-5951
Number of pages13
Issue number45
StatePublished - Nov 8 2018

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cancer Research


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