Mutation analysis of Rad18 in human cancer cell lines and non small cell lung cancer tissues

作者：Nakamura Tadahiko; Ishikawa Shinji; Koga Yoshikatsu; Nagai Youhei; Imamura Yu; Ikeda Kouei; Mori Takeshi; Nomori Hiroaki; Baba Hideo^*

来源：Journal of Experimental & Clinical Cancer Research, 2009, 28(1): 106.

DOI：10.1186/1756-9966-28-106

Background: Genetic instability is known as a cause of oncogenesis. Though Rad18 is reported to function in a post replication mismatch repair system, the relation between the status of Rad18 and human tumorigenesis has not been described so far.
Methods: Mutation analysis of 34 human cancer cell lines and 32 non small cell lung cancer (NSCLC) tissues were performed by RT-PCR SSCP. Expression level of Rad18 was measured by real time RT-PCR. Stable transfectant was constructed for in vitro study.
Results: No mutation was found in both cancer cell lines and NSCLC tissues. A single nucleotide polymorphism ( SNP) at codon 302 was detected in 51.5% of the cell lines and 62.5% of NSCLC tissues. Interestingly, Rad18 was homozygously deleted in a pulmonary adenocarcinoma cell line PC3. Furthermore, there was no difference in the expression level of wild type Rad18 and Rad18 with SNP. The growth, cell morphology, sensitivity to anti-cancer drugs and in vitro DNA repair activity between wild type Rad18 and Rad18 with SNP revealed to have no difference in vitro.
Conclusion: Though the frequency of SNP was tended to be higher in NSCLC patients than healthy volunteers (57.7%), as the difference was not significant, we have concluded that there is no relation between Rad18 SNP and lung cancer development.

• 出版日期2009-7-25