## Abstract Studies indicate that peroxisome proliferator‐activated receptor‐β/δ (PPARβ/δ) can either attenuate or potentiate colon cancer. One hypothesis suggests that PPARβ/δ is upregulated by the adenomatous polyposis coli (APC)/β‐CATENIN pathway and a related hypothesis suggests that PPARβ/δ is
Erratum: to “Regulation of peroxisome proliferator-activated receptor-β/δ by the APC/β-CATENIN pathway and nonsteroidal anti-inflammatory drugs” by Jennifer E. Foreman, Joseph M. Sorg, Kathleen S. McGinnis, Basil Rigas, Jennie L. Williams, Margie L. Clapper, Frank J. Gonzalez, and Jeffrey M. Peters 2009; 48:942–952.
- Publisher
- John Wiley and Sons
- Year
- 2011
- Tongue
- English
- Weight
- 160 KB
- Volume
- 50
- Category
- Article
- ISSN
- 0899-1987
- DOI
- 10.1002/mc.20782
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✦ Synopsis
In the above-mentioned article, we incorrectly indicated that a non-specific immunoreactive protein was PPARg1, and that an immunoreactive protein with slightly lower relative mobility was PPARg2. Based on re-analysis (Erratum Fig. 1), it is now clear that: (1) only PPARg1 is expressed in our samples, (2) the protein we indicated was PPARg2 is in fact PPARg1, and (3) the protein we indicated was PPARg1 is in fact a non-specific immunoreactive protein. Since the focus of our paper was directed more on the role of PPARb/d in colon cancer rather than PPARg, this clarification only modestly affects our conclusions. Based on this re-analysis, the following points correct our previous interpretation: Á PPARg2 is not expressed in mouse colon. Á PPARg2 is expressed weakly in some human colon cancer cell lines. Á PPARg1 expression is lower in the polyps from Apc min/þ mice as compared to control Apc min/þ colon tissue. Á Expression of PPARg1 (not PPARg2) is higher in HT29 and LS174T human colon cancer cell lines as compared to RKO, DLD1, and HCT116.
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