NDLI: Colonic tumorigenesis in BubR1 +/– Apc Min/+ compound mutant mice is linked to premature separation of sister chromatids and enhanced genomic instability

Content Provider	PubMed Central
Author	Rao, Chinthalapally V. Yang, Yang-ming Swamy, Malisetty V. Liu, Tongyi Fang, Yuqiang Mahmood, Radma Meena, Jhanwar-uniyal Dai, Wei
Copyright Year	2005
Abstract	Faithful chromosome segregation is essential for the maintenance of genetic stability during cell division and it is at least partly monitored by the spindle checkpoint, a surveillance mechanism preventing the cell from prematurely entering anaphase. The adenomatous polyposis coli (Apc) gene also plays an important role in regulating genomic stability, as mutations of Apc cause aneuploidy. Here we show that whereas ApcMin /+ mice developed many adenomatous polyps, mostly in the small intestine, by 3 mo of age; BubR1 +/– ApcMin /+ compound mutant mice developed 10 times more colonic tumors than ApcMin /+ mice. The colonic tumors in BubR1 +/– ApcMin /+ mice were in higher grades than those observed in ApcMin /+ mice. Consistently, BubR1 +/– ApcMin /+ murine embryonic fibroblasts (MEFs) contained more β-catenin and proliferated at a faster rate than WT or BubR1 +/– MEFs. Moreover, BubR1 +/– ApcMin /+ MEFs slipped through mitosis in the presence of nocodazole and exhibited a higher rate of genomic instability than that of WT or BubR1 +/– or ApcMin /+ MEFs, accompanied by premature separation of sister chromatids. Together, our studies suggest that BubR1 and Apc functionally interact in regulating metaphase–anaphase transition, deregulation of which may play a key role in genomic instability and development and progression of colorectal cancer.
Related Links	http://dx.doi.org/10.1073/pnas.0407822102
Ending Page	4370
Page Count	6
Starting Page	4365
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	12
Volume Number	102
Language	English
Publisher	National Academy of Sciences
Publisher Date	2005-03-22
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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Colonic tumorigenesis in BubR1+/-ApcMin/+ compound mutant mice is linked to premature separation of sister chromatids and enhanced genomic instability.

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Colonic tumorigenesis in BubR1+/-ApcMin/+ compound mutant mice is linked to premature separation of sister chromatids and enhanced genomic instability.

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