PRIP promotes tumor formation through enhancing serum-responsive factor-mediated FOS expression

Yiwei Tony Zhu, Liping Hu, Chao Qi, Yi Jun Zhu*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

8 Scopus citations

Abstract

PRIP (peroxisome proliferator-activator receptor interacting protein) is a nuclear receptor coactivator required for mammary gland development. To understand the function of PRIP in breast tumorigenesis, we established a mammary tumor cell line with the PRIPLoxp/Loxp genotype. By knocking out the PRIP gene in the tumor cell line, we demonstrated that PRIP deficiency led to inhibited tumor formation without affecting tumor cell proliferation. The PRIP deficiency was associated with decreased cell invasion and migration capabilities. We found that PRIP deficiency substantially reduced FOS gene expression. A chromatin immunoprecipitation assay revealed that PRIP was recruited to the FOS promoter. In addition, we demonstrated that PRIP also directly up-regulated the FOS gene expression in human breast cancer cells. Promoter analysis showed that PRIP acted through serum-responsive factor to regulate FOS gene expression. Finally, by re-expressing the FOS gene, we confirmed that the inhibited tumor formation of PRIP-deficient tumor cells was due to reduced expression of the FOS gene.

Original languageEnglish (US)
Pages (from-to)14485-14492
Number of pages8
JournalJournal of Biological Chemistry
Volume284
Issue number21
DOIs
StatePublished - May 22 2009

ASJC Scopus subject areas

  • Molecular Biology
  • Biochemistry
  • Cell Biology

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