Work by University of California Researchers has paved way in identification of Bmi-1 protein that results in the transformation of healthy cells into prostrate cancer cells. Bmi-1 protein in prostate cell plays a critical role in regulation of normal prostate cells, repairing worn out cells and recovering normal cells killed by hormone withdrawal therapy.
The findings, by researchers with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, may have important implications for controlling cancer growth and progression.
The protein, called Bmi-1, is often up-regulated in prostate cancer, has been associated with higher grade cancers and is predictive of poor prognosis, according to previous studies.
However, its functional roles in prostate stem cell maintenance and prostate cancer have been unclear, said Owen Witte, senior author of the study.
Prostate cancer
A study of loss and gain of function in prostate stem cells indicated that Bmi-1 expression was required for self-renewal activity and maintenance of prostate stem cells with highly proliferative abilities.
Loss of Bmi-1 expression blocks the self-renewal activity, protecting prostate cells from developing abnormal growth changes which can lead to cancer.
More importantly, Bmi-1 inhibition slowed the growth of an aggressive form of prostate cancer in animal models, in which the PTEN tumor suppressor gene was removed allowing the cancer to run wild, Witte said.
“We conclude by these results that Bmi-1 is a crucial regulator of self-renewal in adult prostate cells and plays important roles in prostate cancer initiation and progression.
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