PPARγ agonists target aromatase via both PGE2 and BRCA1

Ofer Margalit, Dingzhi Wang, Raymond N. DuBois

    Research output: Contribution to journalReview articlepeer-review

    13 Scopus citations


    Obesity is a well-recognized risk factor for postmenopausal breast cancer. Although the underlying mechanisms are not clearly defined, aromatase is thought to play a pivotal role in connecting obesity-associated inflammation with postmenopausal breast cancer. It has been well established that both the proinflammatory prostaglandin E2 (PGE2) and the BRCA1 tumor-suppressor gene regulate aromatase expression. In this issue of the journal (beginning on p. 1183), Subbaramaiah and colleagues improve our understanding of the molecular mechanisms by which PPARγ inhibits aromatase expression. They found that pioglitazone, a PPARγ agonist, inhibited aromatase expression by inhibition of PGE2 signaling and upregulation of BRCA1. Their findings provide potential targets for preventing or treating obesity-related breast cancer.

    Original languageEnglish (US)
    Pages (from-to)1169-1172
    Number of pages4
    JournalCancer Prevention Research
    Issue number10
    StatePublished - Oct 2012

    ASJC Scopus subject areas

    • Oncology
    • Cancer Research


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