HMGA-targeted phosphorothioate DNA aptamers increase sensitivity to gemcitabine chemotherapy in human pancreatic cancer cell lines |
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Authors: | Watanabe Miki Sheriff Sulaiman Lewis Kenneth B Tinch Stuart L Cho Junho Balasubramaniam Ambikaipakan Kennedy Michael A |
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Affiliation: | a Department of Chemistry and Biochemistry, Miami University, Oxford, OH 45056, United States b Department of Surgery, University of Cincinnati Medical Center, Cincinnati, OH, United States c Shriners Hospital for Children, Cincinnati, OH 45229, United States d Cincinnati Veterans Affairs Medical Center, Cincinnati, OH 45220, United States |
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Abstract: | Elevated high mobility group A (HMGA) protein expression in pancreatic cancer cells is correlated with resistance to the chemotherapy agent gemcitabine. Here, we demonstrate use of HMGA-targeted AT-rich phosphorothioate DNA (AT-sDNA) aptamers to suppress HMGA carcinogenic activity. Cell growth of human pancreatic cancer cells (AsPC-1 and Miapaca-2) transfected with AT-sDNA were monitored after treatment with gemcitabine. Significant increases in cell death in AT-sDNA transfected cells compared to non-AT-rich sDNA treated cells were observed in both cell lines. The data indicate the potential use of HMGA targeted DNA aptamers to enhance chemotherapy efficacy in pancreatic cancer treatment. |
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Keywords: | ATfDNA, fluorescence labeled DNA AT-sDNA, AT-rich phosphorothioate DNA CG-sDNA, CG-rich phosphorothioate DNA DMEM, Dulbecco&rsquo s Modified Eagle Medium DNaseI, Deoxyribonuclease I EMSA, electrophoretic mobility shift assay FBS, fetal bovine serum HMGA, high mobility group A IC50, half maximal inhibitory concentration IPTG, isopropyl β-D-1-thiogalactopyranoside Mix-sDNA, random sequence phosphorothioate DNA sDNA, phosphorothioate DNA TAE, Tris base, acetic acid and EDTA buffer |
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