Spindle assembly abnormal
protein 6 homolog (SASS6) plays an important role in the regulation of centriole duplication. To date, the genetic alteration of SASS6 has not been reported in human
cancers. In the present study, we examined whether SASS6 expression is abnormally regulated in
colorectal cancers (
CRCs). Increased SASS6
mRNA and
protein expression levels were observed in 49 (60.5%) of the 81 primary
CRCs and 11 (57.9%) of the 19 primary
CRCs, respectively. Moreover, the upregulation of SASS6
mRNA expression was statistically significant (P=0.0410). Next, using DLD-1
colon cancer cells inducibly expressing SASS6, SASS6 overexpression was shown to induce centrosome amplification, mitotic abnormalities such as chromosomal misalignment and lagging chromosome, and chromosomal numerical changes. Furthermore, SASS6 overexpression was associated with anaphase bridge formation, a type of mitotic structural abnormality, in primary
CRCs (P<0.01). SASS6 upregulation in
colon cancer was also revealed in the
Cancer Genome Atlas (TCGA) data and was shown to be an independent predictor of poor survival (multivariate analysis: hazard ratio, 2.805; 95% confidence interval, 1.244‑7.512; P=0.0112). Finally, further analysis of the TCGA data demonstrated SASS6 upregulation in a modest manner in 8 of 11
cancer types other than
colon cancer, and SASS6 upregulation was found to be associated with a poor survival outcome in patients with kidney
renal cell carcinoma and
lung adenocarcinoma. Our present findings revealed that the upregulation of SASS6 expression is involved in the pathogenesis of CRC and is associated with a poor prognosis among patients with
colon cancer. They also suggest that SASS6 upregulation is a genetic abnormality relatively common in human
cancer.