甲醛致大鼠鼻腔癌与K-ras癌基因活化相关

为探讨甲醛致大鼠鼻腔癌的分子机制,对甲醛诱发的大鼠鼻腔癌细胞系FAT7中的转化序列进行检测.采用的实验方法,包括肿瘤细胞DNA与选择标志基因(neo)共转染、裸鼠成瘤性分析、Southern杂交、聚合酶链反应(PCR)和序列分析等.结果发现:在第二轮裸鼠肿瘤DNA中含有大鼠源性的K-ras基因序列,而无大鼠源性的H-ras、N-ras和p53基因序列.这表明甲醛诱发的大鼠鼻腔癌细胞系FAT7中所含的转化序列与H-ras、N-ras及p53基因无关,K-ras癌基因的活化可能参与甲醛致大鼠鼻腔癌.

Involvement of K-ras Oncogene Activation in Formaldehyde-induced Rat Nasal Carcinoma

To further explore the molecular mechanism involved in pathogenesis of formaldehyde-induced rat nasal carcinoma,the transforming sequence was detected in FAT7,a cell line derived from rat nasal carcinoma induced by formaldehyde.Several methods,such as co-transfection of tumor DNA and selectable marker gene (neo),nude mice tumorigenicity assay,Southern hybridization,polymerase chain reaction (PCR) and sequence analysis were applied in this study.The results showed that a rat original K-ras oncogene sequence was found in genomic DNAs from the tumors in nude mice by PCR and sequencing,but no rat H-ras,N-ras and p53 gene sequence was detected.It was indicated that the activation of rat K-ras oncogene,but absence of H-ras,N-ras and p53 gene activation,might be involved in the development of formaldehyde-induced rat nasal carcinoma.