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Brief Report
Daxx Shortens Mitotic Arrest Caused by Paclitaxel
Cory R. Lindsay, Axel Scholz, Viacheslav M. Morozov and Alexander M. Ishov
volume 6 | issue 10
15 May 2007Pages: 1200 - 1204
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Resistance to anti-neoplastic drug paclitaxel is frequent in breast cancer patients. Most studies of paclitaxel resistance have focused on pathways that elicit cellular response, while little is known about players involved in the acquirement of taxane resistance. By screening a cohort of breast cancer cell lines, we observed a correlation between level of protein Daxx and response to paclitaxel. Cells lines expressing increased level of Daxx displayed a robust paclitaxel response with nearly all cells undergoing micronucleation, while cell lines with low amount of Daxx showed a decrease in micronucleation, and accumulation in mitosis. At used paclitaxel concentrations, apoptotic levels were negligible in all cell lines tested. Human cell lines expressing anti-Daxx siRNA as well as Daxx-/- mouse fibroblasts showed similar cellular response to paclitaxel. Importantly, absence or depletion of Daxx resulted in cell survival after paclitaxel treatment, as measured by colony formation assay. We conclude that Daxx may be an important predictive factor in cellular response to paclitaxel, which emphasizes a critical but unknown function of this protein in mitotic progression, which, when disabled, leads to survival advantages upon paclitaxel treatment.
Authors
Cory R. Lindsay
University of Florida, Gainesville, Florida
Axel Scholz
University of Florida, Gainesville, Florida
Viacheslav M. Morozov
University of Florida, Gainesville, Florida
Alexander M. Ishov
University of Florida, Gainesville, Florida
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.