Haruki N, Saito H, Harano T, Nomoto S, Takahashi T, Osada H, Fujii Y, Takahashi T
Laboratory of Ultrastructure Research, Pathophysiology Unit, Aichi Cancer Center Research Institute, 1-1 Kanokoden, Chikusa-ku, 464-8681, Nagoya, Japan.
Cancer Lett. 2001 Jan 26;162(2):201-5. doi: 10.1016/s0304-3835(00)00675-3.
Our previous studies showed that mitotic checkpoint impairment is present in about 40% of human lung cancer cell lines but that mutations in the MAD mitotic checkpoint genes are infrequent. In the present study, we examined 44 lung cancer cases for the potential involvement of the other gene family involved in the mitotic checkpoint, i.e. BUB. We found that the BUB gene family members including BUB1, BUBR1 and BUB3 are not frequent targets for mitotic checkpoint defects in lung cancers, if present at all. Further studies are thus warranted to elucidate the molecular basis for the acquisition of mitotic checkpoint defects in order to better understand the molecular pathogenesis of lung cancers.
我们之前的研究表明,约40%的人肺癌细胞系存在有丝分裂检查点缺陷,但MAD有丝分裂检查点基因的突变并不常见。在本研究中,我们检测了44例肺癌病例,以探究参与有丝分裂检查点的另一个基因家族(即BUB)的潜在作用。我们发现,包括BUB1、BUBR1和BUB3在内的BUB基因家族成员,即便在肺癌中存在,也并非有丝分裂检查点缺陷的常见靶点。因此,有必要进一步开展研究以阐明获得有丝分裂检查点缺陷的分子基础,从而更好地理解肺癌的分子发病机制。