@article{oai:kindai.repo.nii.ac.jp:00020203,
 author = {塩浜, 康雄 and Shihama,Yasuo and 藤田, 崇史 and Fujita,Takashi and 神武, 洋二郎 and Kotake,Yojiro and 岡田, 斉 and Okada,Hitoshi and 藤井, 政幸 and Fujii,Masayuki},
 issue = {30},
 journal = {かやのもり：近畿大学産業理工学部研究報告, Reports of Faculty of Humanity-Oriented Science and Engineering, Kindai University},
 month = {Jun},
 note = {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., application/pdf},
 pages = {1--7},
 title = {〈論文・報告〉siRNAによる変異癌遺伝子KRAS(G12D)の選択的発現制御},
 year = {2019},
 yomi = {シハマ, ヤスオ and フジタ, タカシ and コウタケ, ヨウジロウ and オカダ, ヒトシ and フジイ, マサユキ}
}