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. Author manuscript; available in PMC: 2013 Jul 1.
Published in final edited form as: Mol Cancer Ther. 2012 May 2;11(7):1587–1597. doi: 10.1158/1535-7163.MCT-11-1058

Figure 5. Knockdown of Smo diminishes HH pathway activity, reduces viability and reverses taxane resistance in ovarian cancer cells.

Figure 5

A) A2780cp20 cells were exposed to either control or Smo siRNA for 72 hours and examined for mRNA expression of HH pathway mediators SMO, PTCH1, GLI1 and GLI2. *P < 0.01, compared to control siRNA. Protein expression of Smo and Gli (inset) was also measured using Western blot analysis to confirm mRNA results. β-actin was used as a loading control. A2780cp20 cells were transfected with either control siRNA or 2 distinct siRNA constructs designed against Smo (B), Gli1 (C) or Gli2 (D) and exposed to increasing concentrations of paclitaxel. Cell viability was determined by MTT assay. Data are representative of 3 independent experiments.