日本語フィールド
著者：Toshimi Hoshiko, Yasushi Kubota, Takuya Akisawa, Tatsuro Watanabe, Kazuaki Tanigawara, Junichi Yano, Shinya Kimura題名：Naked antisense double-stranded DNA oligonucleotide efficiently suppresses BCR-ABL positive leukemic cells発表情報：Invest New Drugs 巻: 38 号: 4 ページ: 1012-1019キーワード：概要：Oligonucleotide-based gene silencing, using molecules such as antisense oligonucleotides (ASOs), small interfering RNA, and aptamers, is widely studied. Another approach uses DNA/RNA heteroduplex oligonucleotides (HDOs). Here, we developed an antisense double-stranded DNA oligonucleotide (ADO) by modification of the complementary RNA in an HDO to generate DNA for increasing resistance to nucleases. Naked BCR-ABL-targeting ADO was significantly more potent than siRNA at reducing BCR-ABL chimeric mRNA expression in chronic myeloid leukemia (CML) cell lines. Further, naked BCR-ABL-targeting ADO suppressed BCR-ABL protein levels in a dose-dependent manner, inhibited CML cell proliferation, and augmented the inhibitory effects of imatinib mesylate. In conclusion, ADO technology is an attractive method for therapeutic application.抄録：英語フィールド
Author：Toshimi Hoshiko, Yasushi Kubota, Takuya Akisawa, Tatsuro Watanabe, Kazuaki Tanigawara, Junichi Yano, Shinya KimuraTitle：Naked antisense double-stranded DNA oligonucleotide efficiently suppresses BCR-ABL positive leukemic cellsAnnouncement information:Invest New Drugs Vol: 38 Issue: 4 Page: 1012-1019An abstract：Oligonucleotide-based gene silencing, using molecules such as antisense oligonucleotides (ASOs), small interfering RNA, and aptamers, is widely studied. Another approach uses DNA/RNA heteroduplex oligonucleotides (HDOs). Here, we developed an antisense double-stranded DNA oligonucleotide (ADO) by modification of the complementary RNA in an HDO to generate DNA for increasing resistance to nucleases. Naked BCR-ABL-targeting ADO was significantly more potent than siRNA at reducing BCR-ABL chimeric mRNA expression in chronic myeloid leukemia (CML) cell lines. Further, naked BCR-ABL-targeting ADO suppressed BCR-ABL protein levels in a dose-dependent manner, inhibited CML cell proliferation, and augmented the inhibitory effects of imatinib mesylate. In conclusion, ADO technology is an attractive method for therapeutic application.