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Knockdown of peroxisome proliferator-activated receptor-β induces less differentiation and enhances cell-fibronectinadhesion of colon cancer cells
Linköping University.
Linköping University.
Linköping University.
Linköping University.
Vise andre og tillknytning
2010 (engelsk)Inngår i: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 29, nr 4, s. 516-526Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The role of peroxisome proliferator-activated receptor-/ (PPAR-/) in the pathogenesis of colon cancer remains highly controversial. This study specifically silenced the PPAR- expression in three colon cancer cell lines with different metastatic potentials. Although PPAR-knockdown resulted in more malignant morphological changes, bigger colony sizes and lower carcinoembryonic antigen (CEA) secretion, and enhanced the cell-fibronectin adhesion, cell invasion and migration were unaffected. These effects were stronger in poorly metastatic cell lines compared with highly metastatic ones. Simultaneously, PPAR-knockdown decreased the mRNAs encoding adipocyte differentiation-related protein and liver fatty acid binding protein, and increased the mRNA of ILK, whereas the mRNAs encoding integrin-1 and angiopoietin-like 4 were unchanged. Using immunohistochemistry, we determined that the intensity of PPAR- expression was stronger in rectal cancers with better differentiation than in those with poor differentiation, and was stronger in early-stage tumors than in advanced ones. Together, these findings consistently indicate that PPAR- may facilitate differentiation and inhibit the cell-fibronectin adhesion of colon cancer, having a role as an inhibitor in the carcinogenesis and progression of colorectal cancer. Interestingly PPAR- seems to have a more important role in poorly metastatic cells than in highly metastatic ones.

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Nature publishing group , 2010. Vol. 29, nr 4, s. 516-526
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URN: urn:nbn:se:his:diva-3661DOI: 10.1038/onc.2009.370ISI: 000274084600005Scopus ID: 2-s2.0-75749150060OAI: oai:DiVA.org:his-3661DiVA, id: diva2:292506
Tilgjengelig fra: 2010-02-08 Laget: 2010-02-08 Sist oppdatert: 2017-12-12bibliografisk kontrollert

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