An Overview of the Spindle Assembly Checkpoint Status in Oral Cancer

Abstract

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.

Arabidopsis Cell Division Cycle 20.1 Is Required for Normal Meiotic Spindle Assembly and Chromosome Segregation

“…The faithful segregation of genetic material into daughter cells during cell division is crucial for the production of healthy progeny (Jin et al, 2010;Whitfield et al, 2013;Teixeira et al, 2014). Chromosome segregation is regulated by several mechanisms, including cohesion degradation and SAC-dependent surveillance (Musacchio and Ciliberto, 2012).…”

Clinicopathologic significance of BubR1 and Mad2 overexpression in oral cancer

“…Several studies reported that defects in SAC activity are linked to an increased rate of aneuploidization during tumorigenesis and that the expression levels of SAC proteins are altered in various human tumours and cell lines (Barbosa et al , ; Silva et al , ). However, our knowledge on SAC protein expression in oral cancer remains rather scarce (Teixeira et al , ). This study aimed at: (i) investigating the expression levels of BubR1 and Mad2 and its relationship to the competence of the SAC in OSCC cell lines; (ii) analysing the expression of BubR1 and Mad2 in OSCC tissue samples; and (iii) evaluating its clinicopathological significance.…”

Previous infection with SARS‐CoV‐2 impacts embryo morphokinetics but not clinical outcomes in a time‐lapse imaging system

“…A possible intrinsic repair mechanism cannot be discarded. Mitotic defects caused by environmental insults, such as viral infection, are monitored by the spindle assembly checkpoint, an evolutionarily conserved mechanism (Teixeira et al, 2014) that participates in a cascade of events that allows more time for cells to correct meiotic defects (Lawrence et al, 2015).…”