Twist overexpression promotes chromosomal instability in the breast cancer cell line MCF-7.
Twist overexpression promotes chromosomal instability in the breast cancer cell line MCF-7.
复制标题
Twist 过度表达会促进乳腺癌细胞系 MCF-7 中的染色体不稳定。
DOI：
10.1016/j.cancergencyto.2006.01.014
复制
发表时间：
2006
影响因子：
--
通讯作者：
Raman,Venu
中科院分区：
文献类型：
--
作者：
Vesuna,Farhad;WinnardJr,Paul;Glackin,Carlotta;Raman,Venu
Erroneous expression of genetic information is a characteristic of a transformed phenotype in cancer biogenesis [1]. The degree of chromosomal instability in a cell can determine its fate toward proliferation or cell death. Chromosomal instability manifests as aneuploidy (loss or gain of chromosomes) or as a rearrangement of chromosomal structure. For example, in human Burkitt’s lymphoma, the C-MYC oncogene is translocated downstream of the enhancer of the immunoglobulin heavy chain gene, resulting in overexpression of C-MYC, which increases both the rate of cell division and chromosomal instability [2]. The translocation resulting in the production of the chimeric BCR-ABL fusion protein has been demonstrated to transform hematopoietic cells, resulting in chronic myelogenous leukemia in humans [3]. Thus, chromosomal aberrations can result in overexpression of oncogenes or suppression of tumor suppressor genes, which in turn promote oncogenic transformation.Fluorescence cytogenetic methods have been well established as a way of studying chromosomal instability, and include techniques such as spectral karyotyping (SKY) and comparative genomic hybridization (CGH). SKY permits the simultaneous visualization of each mammalian chromosome in a different fluorescent color, facilitating the identification of both structural and numerical chromosomal aberrations [4–6]. CGH reveals the different hybridization patterns of labeled tumor versus control (reference) DNA and generates a map of DNA copy number changes in tumor genomes [7]. CGH has been consistently used to characterize chromosomal aberrations in solid tumors and hematologic malignancies in patients [8, 9]. It is very challenging, however, to develop a tumor model system that will allow for the correlation between the function (s)/expression of a particular protein in vivo and its ability to induce chromosomal instability. This is primarily due to the fact that tumors are heterogeneous and the phenotype observed results from the interplay of a number of proteins acting in concert.
