BUBR1 and cancer
The original article in this thread explains some recent results concerning the BubR1 mitotic checkpoint protein and ageing. Defects in this protein have been associated with chromosomal instability (CIN) which contributes to cancers with variation in centromere copy number. The article describes results that suggest high levels of BubR1 confer a survival advantage in mouse models of lung and skin cancer. However the biomedical literature contains several examples in which elevated BubR1 appears to be associated with tumour development and poor prognosis, so there is some confusion as to the role of this protein in cancer which requires further research before it can be fully elucidated.
For example, in a study on human urothelial bladder carcinomas, it was found that in tumours in which there was high expression of BUBR1, there was also CIN, DNA aneuploidy, and centrosome amplification, associated with advanced pathological stage and poor outcomes including tumour recurrence and disease progression. Similarly to bladder cancer, in glioblastoma (GBM) cell lines and tumour samples, increased expression of BUB and BUBR1 was also observed. Upon reduction of BUBR1 expression with siRNA, there was decreased cell proliferation and colony formation and sensitisation of cells to γ-irradiation. Meanwhile studies on hepatocellular carcinoma (HCC) suggested that while high levels of BUBR1 was not uniform across HCCs, being overexpressed in about 45% HCCs, however where it was observed it correlated with increased tumour size and similarly to bladder cancer, higher histological grade, advanced pathology, increased recurrence and lower survival rates. Higher BUBR1 was also associated with p53 expression and with high levels of the proliferation marker Ki67 in HCC tissues.
Clearly on-going research on BUBR1 and cancer and ageing is essential.
Sources
LIU, A. et al., 2009. The clinicopathological significance of BUBR1 overexpression in hepatocellular carcinoma. Journal of clinical pathology, 62(11), pp. 1003-1008
MORALES, A.G. et al., 2013. BUB1 and BUBR1 inhibition decreases proliferation and colony formation, and enhances radiation sensitivity in pediatric glioblastoma cells. Springer Verlag.
YAMAMOTO, Y. et al., 2007. Overexpression of BUBR1 is associated with chromosomal instability in bladder cancer. Cancer genetics and cytogenetics, 174(1), pp. 42-47
The original article in this thread explains some recent results concerning the BubR1 mitotic checkpoint protein and ageing. Defects in this protein have been associated with chromosomal instability (CIN) which contributes to cancers with variation in centromere copy number. The article describes results that suggest high levels of BubR1 confer a survival advantage in mouse models of lung and skin cancer. However the biomedical literature contains several examples in which elevated BubR1 appears to be associated with tumour development and poor prognosis, so there is some confusion as to the role of this protein in cancer which requires further research before it can be fully elucidated.
For example, in a study on human urothelial bladder carcinomas, it was found that in tumours in which there was high expression of BUBR1, there was also CIN, DNA aneuploidy, and centrosome amplification, associated with advanced pathological stage and poor outcomes including tumour recurrence and disease progression. Similarly to bladder cancer, in glioblastoma (GBM) cell lines and tumour samples, increased expression of BUB and BUBR1 was also observed. Upon reduction of BUBR1 expression with siRNA, there was decreased cell proliferation and colony formation and sensitisation of cells to γ-irradiation. Meanwhile studies on hepatocellular carcinoma (HCC) suggested that while high levels of BUBR1 was not uniform across HCCs, being overexpressed in about 45% HCCs, however where it was observed it correlated with increased tumour size and similarly to bladder cancer, higher histological grade, advanced pathology, increased recurrence and lower survival rates. Higher BUBR1 was also associated with p53 expression and with high levels of the proliferation marker Ki67 in HCC tissues.
Clearly on-going research on BUBR1 and cancer and ageing is essential.
Sources
LIU, A. et al., 2009. The clinicopathological significance of BUBR1 overexpression in hepatocellular carcinoma. Journal of clinical pathology, 62(11), pp. 1003-1008
MORALES, A.G. et al., 2013. BUB1 and BUBR1 inhibition decreases proliferation and colony formation, and enhances radiation sensitivity in pediatric glioblastoma cells. Springer Verlag.
YAMAMOTO, Y. et al., 2007. Overexpression of BUBR1 is associated with chromosomal instability in bladder cancer. Cancer genetics and cytogenetics, 174(1), pp. 42-47
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