Scientists discover role for c-myc gene in tumor angiogenesis
The c-myc gene is commonly activated in a variety of human tumors. As a new report in the October 1 issue of Genes & Development shows, scientists are gaining a better understanding as to why.
Dr. John Cleveland and colleagues at St. Jude Childrens Research Hospital have discovered that c-Myc is essential for tumor development, as it regulates factors necessary for the growth of blood vessels into tumors – lending a new potential target to anti-angiogenic cancer therapies.
The myc family of oncogenes (c-myc, N-myc, and L-myc) function in the control of cell proliferation, differentiation, and tumorigenesis. Although it has long been recognized that c-Mycs positive effect on cell proliferation can contribute to cancer development, scientists have also suspected that c-Myc has additional roles in the progression of malignancy. Dr. Cleveland and colleagues have discovered such a role: c-Myc is essential for tumor angiogenesis.
Growing tumors need oxygen and nutrients to survive. Once a tumors demand for oxygen and nutrients exceeds what the existing vasculature can provide, a new vascular network is established (vasculogenesis) and capillaries are formed (angiogenesis) to meet the tumors increasing needs. Since the late nineties, when the first anti-angiogenic drugs entered clinical trials, much interest has centered upon the therapeutic approach to thwart a tumors growth by cutting off its blood supply. By showing that c-Myc is essential for promoting vasculo- and angiogenesis, Dr. Cleveland and colleagues have uncovered another possible route in this anti-angiogenic strategy.
“The goal of this study was to determine the role of c-Myc in development. These studies established that c-Myc is essential for the formation of the vasculature that distributes blood throughout the organism, and that it did so by functioning as a master regulator of factors that are necessary for the growth of blood vessels and capillaries. The surprising result was that these studies also revealed why MYC family genes are activated in 70% of all human cancers,” explains Dr. Cleveland.
To evaluate the physiological role of c-Myc, Dr. Cleveland and colleagues re-derived a strain of transgenic mice that are deficient in the gene. The c-myc-deficient mice die as embryos due to cardiac and neural defects, but also display marked defects in vasculogenesis, angiogenesis, and the formation of red blood cells. The researchers found that the vascular defects in the c-Myc-deficient mice arise from the mis-expression of intercellular signals that coordinate vasculo- and angiogenesis during development.
Drs. Cleveland and Baudino and colleagues went on to show that c-Myc plays a similar role in orchestrating vasculogenesis during tumor formation. The researchers demonstrated that c-Myc-deficient embryonic stem cells have a diminished ability to form tumors in immunocompromised mice, and that the small tumors that sometimes form have dramatically less vasculature. Further delineation of role of c-Myc in promoting human tumorigenesis is needed, but as it stands, this study presents strong evidence to suggest that the disruption of c-Myc may prove successful as an anti-angiogenic tool in cancer therapy.
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