@article{oai:kanazawa-u.repo.nii.ac.jp:00026814,
 author = {加治, 正英 and 米村, 豊 and 廣野, 靖夫 and 津川, 浩一郎 and 伏田, 幸夫 and 藤村, 隆 and 三輪, 晃一 and 宮崎, 逸夫},
 issue = {4},
 journal = {日本消化器外科学会雑誌 = The Japanese journal of gastroenterological surgery},
 month = {Apr},
 note = {標的mRNAに選択的に結合するDNAを用いて遺伝子発現をブロックする方法がアンチセンス法である. 今回, 癌の進展に関与するc-met遺伝子に対して, 胃癌培養細胞における発現異常と, アンチセンスDNAによる培養細胞の増殖および浸潤抑制について検討した. c-met遺伝子の発現を Northern blotにて解析したところ, c-met mRNAレベルはMKN-45>TMK-1>MKN-28の順に高かった. MKN-45細胞の増殖は10μMアンチセンスDNAの存在下で90%以上抑制された. マトリゲル中へのTMK-1細胞浸潤は, c-metアンチセンスDNA存在下で濃度依存性に低下した. 以上の結果から, c-metに対するアンチセンスDNAが胃癌の進展阻止のための有効な治療手段となる可能性も考えられた. We first screened for c-met expression in human gastric cancer cell lines, MKN-28, MKN-45 and TMK-1, by Northern blot analysis. The rank order of c-met mRNA abundance in these cell lines was MKN.45>TMK-1>MKN-28. Next, to test whether the growth and invasion of gastric cancer cells depend on c-met, we prepared phosphorothioate-type antisense oligonucleotides that were complementary to human c-met mRNA. We conducted experiments to determine whether blocking expression of the c-met gene with the antisense molecules affected either the proliferative or the invasive phenotype of the cancer cells. The growth of MKN-45 cells was markedly inhibited by the antisense c-met oligonucleotides, in a dose-dependent manner, but not by sense controls. The antisense oligonucleotides also effectively inhibited the migration of TMK-1 cells. These results indicate that c-met gene products may be causally related to the proliferation or invasion of gastric cancer cells, and that antisense c-met DNA has therapeutic potential in that it may facilitate circumventing the progression of gastric cancers.},
 pages = {910--914},
 title = {C-metアンチセンスDNAによるヒト胃癌細胞の増殖・浸潤抑制の検討},
 volume = {30},
 year = {1997}
}