Liang Qian-Jin, Lu Xiang-Feng, Cheng Xiao-Lei, Luo Song, He Da-Cheng, Wang Yong-Chao
College of Life Sciences, Beijing Normal University, Beijing 100875, China.
Yi Chuan Xue Bao. 2004 Mar;31(3):236-40.
At present, a point that cell biologists and medicine scientists focus their close attention on is the mechanisms of cell proliferation and carceration. Breast cancer, one of the frequently occurring cancers, is often been studied intensively. Centromere constitutive molecules, related to various regulatory factors, play an important role in cell proliferation check point regulation. Cell cycle engine molecules, oncogenes, anti-oncogenes and other molecules conform a cell proliferation network. The basic courses of all tumors are associated to this network. However, there are still many problems to be resolved in the analyses of cancer related genes which cause tumors and tumor gene markers. In the current study, using Northern blot, 31 samples of breast cancer tissues and their normal (not cancerous) tissues a little far away from them in the same individuals showed that, in the majority of the tests (87.1%), the mRNA of centromere protein CenpB over expressed in breast cancer tissues, and moreover, tissue in situ hybridization also revealed that all of the CenpB-over-expressed cancer tissues, having identified with Northern blot, over expressed CenpB mRNA. Analyzing the same samples by means of Western blot, the result was highly consistent to the studies in the RNA level. A conclusion was drawn that the over expression of CenpB gene probably relates to malignant cell proliferation in breast gland. It has been testified by researchers that a few of CenpB homogenous proteins are co-operative, the loss of their genes resulting in chromosomes' separating abnormally and cell growth's slowing down. Having transfected HeLa (Tet-Off) cells with anti-sense Cenp in a previous experiment, we ever got a result that cellular duplicating time was prolonged for another 32.8 h, and together with the inhibition of centromere assembly, the mitotic index dropped sharply. In another research, we drew a conclusion that CenpG may be related to cancer, and its differential expressing probably relates to malignant cell proliferation. Combined with these researches, the results obtained from the current study are beneficial to further recognition of the mechanism of cancer.
目前,细胞生物学家和医学科学家密切关注的一个点是细胞增殖和癌变的机制。乳腺癌是常见癌症之一,经常受到深入研究。与各种调节因子相关的着丝粒组成分子在细胞增殖检查点调节中起重要作用。细胞周期引擎分子、癌基因、抗癌基因和其他分子构成一个细胞增殖网络。所有肿瘤的基本过程都与这个网络相关。然而,在分析导致肿瘤的癌症相关基因和肿瘤基因标志物方面仍有许多问题有待解决。在当前的研究中,使用Northern印迹法,对31例乳腺癌组织及其在同一个体中距离稍远的正常(非癌)组织进行检测,结果显示,在大多数检测(87.1%)中,着丝粒蛋白CenpB的mRNA在乳腺癌组织中过度表达,此外,组织原位杂交也显示,所有经Northern印迹法鉴定为CenpB过度表达的癌组织,均过度表达CenpB mRNA。通过Western印迹法对相同样本进行分析,结果与RNA水平的研究高度一致。得出结论,CenpB基因的过度表达可能与乳腺恶性细胞增殖有关。研究人员已经证实,一些CenpB同源蛋白相互协作,它们基因的缺失会导致染色体分离异常和细胞生长减缓。在之前的实验中,用反义Cenp转染HeLa(Tet-Off)细胞,我们得到的结果是细胞复制时间延长了32.8小时,并且随着着丝粒组装的抑制,有丝分裂指数急剧下降。在另一项研究中,我们得出结论,CenpG可能与癌症有关,其差异表达可能与恶性细胞增殖有关。结合这些研究,当前研究获得的结果有助于进一步认识癌症的机制。