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Molecular Cancer Therapeutics
Molecular Cancer Therapeutics
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Article

The mitotic serine threonine kinase, Aurora-2, is a potential target for drug development in human pancreatic cancer

Sangeeta Rojanala, Haiyong Han, Rubén M. Muñoz, Walden Browne, Raymond Nagle, Daniel D. Von Hoff and David J. Bearss
Sangeeta Rojanala
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Haiyong Han
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Rubén M. Muñoz
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Walden Browne
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Raymond Nagle
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Daniel D. Von Hoff
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David J. Bearss
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DOI:  Published April 2004
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    Figure 1.

    Protein expression of Aurora-2 kinase in pancreatic cancer cell lines. Western blot analysis indicates an up-regulation of 3–4-fold of Aurora-2 in nine different pancreatic cancer cell lines (AsPC-1, BxPC-3, Capan-1, CFPAC-1, HPAF II, Mia PaCa-2, Mutj, Panc-1, and SU.86.86) in comparison with normal diploid foreskin fibroblast cells (Forf). β-actin served as an internal control.

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    Figure 2.

    Aurora-2 kinase expression in pancreatic patient tumors. Real-time PCR of pancreatic patient tumor samples indicates an up-regulation of Aurora-2 mRNA expression in samples 1, 4, 6, 8, and 9 taken directly from patients compared with normal pancreas tissue (N). Normalized ratio is obtained from pancreatic tumor tissue versus normal tissue.

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    Figure 3.

    Immunohistochemistry of pancreatic tissue array. A, an array of paraffin-embedded pancreatic tumor samples. B, a specific pancreatic tumor sample at higher magnification from the array indicates a high level of Aurora-2 protein expression.

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    Figure 4.

    Inhibition of Aurora-2 using antisense oligonucleotides. A, RT-PCR of a human pancreatic tumor cell line (Mia PaCa-2) treated with antisense Aurora-2 at 25, 50, 100, 200, and 400 nm concentrations. Antisense-treated cells indicate a significant inhibition of Aurora-2 expression at 200 nm concentration compared with the scrambled oligonucleotides. B, RT-PCR of time course study of Mia PaCa-2 cells treated with Aurora-2 antisense indicates inhibition of Aurora-2 expression as early as 6 h.

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    Figure 5.

    Inhibiting Aurora-2 arrests cell cycle. A, time-dependent study showing Western blot analysis of protein extracts from pancreatic cell line (Mia PaCa-2) treated with antisense oligonucleotides shows inhibition of Aurora-2 expression at 24 and 48 h. B, following inhibition of Aurora-2 expression using antisense oligonucleotides, the flow analysis indicates a fraction of cells in sub-G1 phase of the cell cycle in the antisense-treated cells compared with the untreated control, indication of cells undergoing apoptosis.

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    Figure 6.

    Inhibiting Aurora-2 expression induces caspase-3 activation. Mia PaCa-2 cells treated with Aurora-2 antisense show an induction of caspase-3 activity at 24 and 48 h. The untreated cells indicate a baseline of caspase-3 activity at 100% at 24 and 48 h. The antisense scrambled cells (AS Scramble) indicate an increase in caspase-3 activity at 24 h (9%) and 48 h (80%) compared with the untreated control cells. However, the antisense-treated (AS Treated) cells show a significant increase in apoptosis compared with the untreated and the antisense scrambled controls. The antisense-treated cells indicate a 20% increase in caspase-3 activity at 24 h and 90% increase at 48 h compared with the scrambled antisense controls.

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Molecular Cancer Therapeutics: 3 (4)
April 2004
Volume 3, Issue 4
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The mitotic serine threonine kinase, Aurora-2, is a potential target for drug development in human pancreatic cancer
Sangeeta Rojanala, Haiyong Han, Rubén M. Muñoz, Walden Browne, Raymond Nagle, Daniel D. Von Hoff and David J. Bearss
Mol Cancer Ther April 1 2004 (3) (4) 451-457;

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The mitotic serine threonine kinase, Aurora-2, is a potential target for drug development in human pancreatic cancer
Sangeeta Rojanala, Haiyong Han, Rubén M. Muñoz, Walden Browne, Raymond Nagle, Daniel D. Von Hoff and David J. Bearss
Mol Cancer Ther April 1 2004 (3) (4) 451-457;
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Molecular Cancer Therapeutics
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