AI Article Synopsis
- A genomic signature for the estrogen-related receptor alpha (ERRα) was used to analyze over 800 breast tumors, showing that higher ERRα activity is linked to shorter disease-free survival for patients.
- This signature also helped predict the effectiveness of the ERRα inhibitor XCT790 in slowing down breast cancer cell growth in laboratory settings.
- Further studies indicated that the Her2/IGF-1R signaling pathways enhance ERRα activity through the stabilization of C-MYC and the upregulation of PGC-1β, with knockdown of PGC-1β leading to decreased ERRα signaling and reduced proliferation of breast cancer cells.
Article Abstract
A genomic signature designed to assess the activity of the estrogen-related receptor alpha (ERRα) was used to profile more than 800 breast tumors, revealing a shorter disease-free survival in patients with tumors exhibiting elevated receptor activity. Importantly, this signature also predicted the ability of an ERRα antagonist, XCT790, to inhibit proliferation in cellular models of breast cancer. Using a chemical genomic approach, it was determined that activation of the Her2/IGF-1R signaling pathways and subsequent C-MYC stabilization upregulate the expression of peroxisome proliferator-activated receptor gamma coactivator-1 beta (PGC-1β), an obligate cofactor for ERRα activity. PGC-1β knockdown in breast cancer cells impaired ERRα signaling and reduced cell proliferation, implicating a functional role for PGC-1β/ERRα in the pathogenesis of breast cancers.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199323 | PMC |
| http://dx.doi.org/10.1016/j.ccr.2011.08.023 | DOI Listing |
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