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. Author manuscript; available in PMC: 2014 Mar 14.
Published in final edited form as: Oncogene. 2011 Jun 6;31(1):13–26. doi: 10.1038/onc.2011.211

Figure 4. Depletion of Daxx or Rassf1 increases taxol resistance and prolongs Cyclin B stability.

Figure 4

A) Western blot analysis of Daxx and Rassf1A depletion in HEp2 cells. B) Colony formation assay of parental, control- Daxx- and Rassf1A-depleted cells exposed to 10 nM taxol for 12, 18, and 24 hrs after release from double thymidine block. Rapid decrease in survival is seen in parental and control cells, while Daxx- and Rassf1A-depleted cells withstood taxol treatment and produced colonies. C) Western blot analysis of cyclin B protein stability in HEp2 control-, Daxx- and Rassf1A-siRNA cell lines treated with taxol for the indicated amount of time (6–22 hrs). Cells were synchronized using a double thymidine block and released (0 hr) into normal media containing 10 nM taxol. The bottom panel: densitometry analysis of cyclin B normalized by actin; for each cell line the cyclin B/actin ratio at 0 hr set as 1.0. Whereas cyclin B protein levels rapidly decrease by 13 hrs post-thymidine release in control shRNA cells, cyclin B protein levels were stabilized longer in Daxx- and Rassf1A-depleted cells (through 22 hrs, post-thymidine release), indicating Daxx and Rassf1A-depletion prolongs exit from mitosis in response to taxol exposure. Data show a representative experiment out of three.