Oyama Go, Midorikawa Toshiaki, Matsumoto Yasutaka, Takeyama Mayu, Yamada Kenji, Nozawa Takaomi, Morikawa Masako, Imai Kazushi
Department of Biochemistry, The Nippon Dental University School of Life Dentistry at Tokyo, 1-9-20 Fujimi, Chiyoda-ku, Tokyo, 102-8159, Japan.
Odontology. 2013 Jul;101(2):150-5. doi: 10.1007/s10266-012-0079-9. Epub 2012 Jul 3.
Oral carcinoma patients with inactivation of mucosa-associated lymphoid tissue 1 (MALT1) expression worsen their prognoses. Although the genetic mutation could be responsible for the inactivation, no information is available at present. In the present study, genomic DNA of oral carcinoma cells (HOC313, TSU, HSC2, HSC3, KOSC2, KOSC3, SCCKN, OSC19, Ca9.22, and Ho1u1 cells) and normal gingival fibroblasts (GF12 cells) derived from a Japanese population were amplified by polymerase chain reaction using primer sets spanning MALT1 exons, and nucleotide substitutions were analyzed by the single strand conformation polymorphism analysis. The substitutions were commonly observed in all cells, which express MALT1 at various levels. The substitutions at exons 1 and 9 were located at the 5' untranslated region and replaced (336)Asp to Asn, respectively, and others were positioned at the introns. Among the intronic substitutions, four were matched with the single nucleotide polymorphisms (SNPs) registered at the database. Since all cells were derived from a Japanese population, all substitutions detected are the SNPs. Absence of the carcinoma cell-specific mutation suggests that the inactivation of MALT1 expression but not the mutation promotes oral carcinoma progression.
黏膜相关淋巴组织1(MALT1)表达失活的口腔癌患者预后较差。虽然基因突变可能是导致失活的原因,但目前尚无相关信息。在本研究中,使用跨越MALT1外显子的引物对,通过聚合酶链反应扩增来自日本人群的口腔癌细胞(HOC313、TSU、HSC2、HSC3、KOSC2、KOSC3、SCCKN、OSC19、Ca9.22和Ho1u1细胞)和正常牙龈成纤维细胞(GF12细胞)的基因组DNA,并通过单链构象多态性分析来分析核苷酸替换情况。这些替换在所有细胞中均普遍存在,这些细胞表达不同水平的MALT1。外显子1和9的替换分别位于5'非翻译区,将(336)天冬氨酸替换为天冬酰胺,其他替换位于内含子。在内含子替换中,有四个与数据库中登记的单核苷酸多态性(SNP)相匹配。由于所有细胞均来自日本人群,检测到的所有替换均为SNP。癌细胞特异性突变的缺失表明,MALT1表达的失活而非突变促进了口腔癌的进展。