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Motor regulatory protein blocked ovarian tumor growth
Pulipati N. Intl J Cancer. 2011;DOI:10.1002/ijc.25954.
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Over-expression of the protein km23-1 caused the death of ovarian cancer cells in mice, according to the results of a recent study.
Results of a previous study showed that km23-1, a subunit of the motor protein dynein that transports checkpoint proteins along the microtubules during mitosis, was defective in nearly half of patients with ovarian cancer.
Researchers in this study by Pulipati et al hypothesized that increased expression of the protein could block tumor growth. They induced over-expression of km23-1 in human ovarian cancer cells placed in mice, causing the cells to produce large amounts of the normal protein and discovered tumors were significantly smaller in the over-expressed mice.
Researchers observed that the one checkpoint protein BubR1, and possibly others, is not transferred properly in the presence of high km23-1 levels. The dynein motor plays a major role in mitosis, and researchers suggest that a checkpoint is stalled during mitosis when km23-1 is over-expressed, leading to cell death.
Based on these results, researchers are exploring ways to mimic km23-1 over-expression using nanotechnology to deliver a drug to the cancer cells, and how to apply these findings in humans.
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