Background: Chromosomal instability (CIN) is recognized as a hallmark of cancer and is caused by a spindle assembly checkpoint disorder or chromosome mis-segregation during mitosis. Although the recent identification of human shugoshin (hSgo1), an important player in proper chromosome segregation, has suggested involvement of hSgo1 in colorectal tumorigenesis, little is known about how it is involved.
Aims: To obtain information about the status of hSgo1 in human colorectal cancer.
Method/results: Among the 46 colorectal cancer cases, hSgo1 mRNA expression was decreased in the tumor tissue in comparison with the corresponding normal tissue (P=0.032). Human Sgo1 down-regulated tumors (T/N ratio<0.5) had preferential location on the left side large bowel rather than on the right side (P=0.012), and a higher variation of centromere numbers revealed by Fluorescence in situ hybridization (FISH). To assess the effects of hSgo1 down-regulation, we performed hSgo1 knockdown by transfecting the diploid HCT116 cell line with a short hairpin RNA expression vector. Human Sgo1 knockdown cells proliferated slowly because of both G2/M arrest and apoptosis (P<0.001), and marked of CIN in the form of aneuploidy (P<0.001) and micronuclei (P<0.005) were later observed in hSgo1 knockdown cells. Increased centrosome amplification (P<0.05), the presence of binucleated cells, and mitotic catastrophes were also noted in hSgo1 knockdown cells.
Conclusions: These findings suggest that hSgo1 down-regulated colorectal cancers have a clinicopathological character of CIN and hSgo1 down-regulation leads to CIN in colorectal cancer cells.
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