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Enzymes that regulate spread of breast cancer

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     For breast cancer cell to get detached from the breast, travel through the circulation, deposition in a distant organ and final growth of the deposited cells, a number of factors and enzymes have to be involved. This is a very complex process involving many genes and gene products.

    Researchers from Virginia Commonwealth University Massey Cancer Center have discovered a new signaling component that controls the spread of breast cancer cells. The movement of breast cancer cells of human beings is influenced towards epidermal growth factor by this component.

    Research data published in the recent issue of issue of the Journal of Biological Chemistry shows that the enzymes sphingosine kinases - SphK1 and SphK2 is stimulated by epidermal growth factor. The progression of breast cancer may depend on epidermal growth factor. The potent lipid mediator, sphingosine-1-phosphate is formed by the enzyme family sphingosine kinases - SphK1 and SphK2. The movement of the breast cancer cells without these kinases is not possible.

    The opinion of the leading author Sarah Spiegel is that better tools could be designed for the treatment of cancers if the spreading of tumor cells or metastasize is understood properly. The Massey Cancer Center Cell Signaling program has Sarah Spiegel, Ph.D., as its co-leader who is also the professor in the VCU Department of Biochemistry.

    The role of sphingosine-1-phosphate in the regulation of cell growth was first discovered by Spiegel and her colleagues about a decade back. She is the pioneer to work on new lipid mediators which is supposed to regulate cell growth and cell death. She is recognized internationally for this work.
    Although the fact that multiple growth factors stimulates SphK1 is known to researchers, the regulation of SphK2 is not very clear. However, for understanding the functions of these enzymes in a better way, this work is being continued by Spiegel and her team.
    Spiegel said that in cancer therapy the potential new targets are sphingosine kinases. Grants from the National Cancer Institute has supported this research.