Aurora B is expressed at high level in primary human colorectal cancers and other cancer cell lines. Overexpression of Aurora B results in multinucleation and polyploidy in human cells. However, down-regulation or overexpression of an inactive form of Aurora B yields the same polyploidization phenomenon. Overexpression of Aurora B also leads to centrosome amplification and increased ploidy, and the absence of p53 exacerbates this phenotype. Nevertheless, Aurora B–induced centrosome amplification is possibly due to other pathways. It has been reported that Aurora B overexpression induces chromosomes lagging in metaphase, chromosome segregation error, and errors in cytokinesis, and thus may play a role in carcinogenesis. Depletion of Aurora B or overexpression of an inactive form in cells would also compromise the spindle checkpoint because the activity of Aurora B is required for checkpoint protein recruitment. Because cytokinesis would also fail without Aurora B activity, it makes a good explanation why down-regulation of Aurora B generates increased ploidy. Furthermore, Aurora B promotes inappropriate cellular mobility, which underlies invasion and metastasis of cancer cells.overexpression or nondegradation mutants could promote anchorage-independent growth in soft agar. However, the molecular mechanism has not yet been elucidated.
Drug targets for cancer: Aurora B research reagents
Other vital drug targets for cancer likeAurora B:
Fu J, Bian M, Jiang Q, et al. Roles of Aurora kinases in mitosis and tumorigenesis[J]. Molecular Cancer Research, 2007, 5(1): 1-10.