WEKO3
アイテム
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〈論文・報告〉siRNAによる変異癌遺伝子KRAS(G12D)の選択的発現制御
https://doi.org/10.15100/0000020203
https://doi.org/10.15100/000002020303785ed9-1ab7-44ff-9394-a1448e3bafbb
名前 / ファイル | ライセンス | アクション |
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AA12013209-20190630-0001.pdf (1.6 MB)
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Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2019-08-23 | |||||
タイトル | ||||||
言語 | ja | |||||
タイトル | 〈論文・報告〉siRNAによる変異癌遺伝子KRAS(G12D)の選択的発現制御 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | 〈PAPERS and REPORTS〉Selective Regulation of Mutant Oncogene KRAS (G12D) by siRNA | |||||
著者 |
塩浜, 康雄
× 塩浜, 康雄× 藤田, 崇史× 神武, 洋二郎× 岡田, 斉× 藤井, 政幸 |
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言語 | ||||||
言語 | jpn | |||||
キーワード | ||||||
主題 | Mutant KRAS Positive Cancer, Nucleic Acid Therapeutics, siRNA | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | departmental bulletin paper | |||||
ID登録 | ||||||
ID登録 | 10.15100/0000020203 | |||||
ID登録タイプ | JaLC | |||||
著者 所属 | ||||||
近畿大学産業理工学部生物環境化学科; 博士研究員 | ||||||
著者 所属 | ||||||
近畿大学産業理工学研究科産業理工学専攻生物環境化学コース | ||||||
著者 所属 | ||||||
近畿大学産業理工学部生物環境化学科; 教授 | ||||||
著者 所属 | ||||||
近畿大学医学部生化学教室; 教授 | ||||||
著者 所属 | ||||||
近畿大学産業理工学部生物環境化学科; 教授 | ||||||
版 | ||||||
出版タイプ | NA | |||||
出版タイプResource | http://purl.org/coar/version/c_be7fb7dd8ff6fe43 | |||||
出版者 名前 | ||||||
出版者 | 近畿大学産業理工学部 | |||||
書誌情報 |
ja : かやのもり:近畿大学産業理工学部研究報告 en : Reports of Faculty of Humanity-Oriented Science and Engineering, Kindai University 号 30, p. 1-7, 発行日 2019-06-30 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 13495801 | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | KRAS mutation is positive in 45% of colon cancer patients, 35% of lung cancer patients, 95% of pancreas cancer patients and 15% of melanoma patients and the patients do not benefit from anti-epidermal growth factor receptor (EGFR) chemotherapy and antibody therapy to have poor prognosis for survival. In colorectal cancer patients, 90 % of KRAS mutations are found in codons 12 and 13 of exon 2. It is highly challenging to target mutant KRAS gene by synthetic small nucleic acids and can be a breakthrough for undruggable cancers. In the present study, we investigated silencing of mutant KRAS(G12D) gene by siRNAs using HeLa cell with wild type KRAS and PK-45H cell with G12D mutation in both alleles. Four types of siRNAs, siRNAG12D(13), G12D(10), G12D(8), G12D(2), targeting mutant KRAS (G12D) mRNA at different positions neighboring the mutation point were investigated. The results indicated siRNAG12D(13) suppressed KRAS(G12D) expression by 90.9% at 100 nM and 75.1% at 1 nM while siRNAG12D(13) suppressed wild type KRAS expression by 55.4% at 100 nM and 23.3% at 1 nM, respectively. It is interesting that siRNAG12D(8) and siRNAG12D(2) suppressed both KRAS(G12D) and wild type KRAS strongly and the selectivity was quite low. It is also to be pointed out that siRNAG12D(10) which has a mutation point adjacent to the cleavage site of the target mRNA suppressed both mutant KRAS(G12D) and wild type KRAS only weekly and did not discriminate the mutant KRAS(G12D) from wild type KRAS. | |||||
言語 | en | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | application/pdf |