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An Overview of the Spindle Assembly Checkpoint Status in Oral Cancer
Author(s) -
José H. Teixeira,
Patrícia Silva,
Rita M. Reis,
Inês Moranguinho Moura,
Sandra Marques,
Joana Fonseca,
Luı́s Monteiro,
Hassan Bousbaa
Publication year - 2014
Publication title -
biomed research international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 126
eISSN - 2314-6141
pISSN - 2314-6133
DOI - 10.1155/2014/145289
Subject(s) - spindle checkpoint , aneuploidy , cancer , chromosome instability , biology , cancer research , genome instability , anaphase , metaphase , chromosome , genetics , kinetochore , gene , cell cycle , dna damage , dna
Abnormal chromosome number, or aneuploidy, is a common feature of human solid tumors, including oral cancer. Deregulated spindle assembly checkpoint (SAC) is thought as one of the mechanisms that drive aneuploidy. In normal cells, SAC prevents anaphase onset until all chromosomes are correctly aligned at the metaphase plate thereby ensuring genomic stability. Significantly, the activity of this checkpoint is compromised in many cancers. While mutations are rather rare, many tumors show altered expression levels of SAC components. Genomic alterations such as aneuploidy indicate a high risk of oral cancer and cancer-related mortality, and the molecular basis of these alterations is largely unknown. Yet, our knowledge on the status of SAC components in oral cancer remains sparse. In this review, we address the state of our knowledge regarding the SAC defects and the underlying molecular mechanisms in oral cancer, and discuss their therapeutic relevance, focusing our analysis on the core components of SAC and its target Cdc20.

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