Membrane vesicles are generally classified into three groups based on their size, surface membrane composition, and mechanism of release from the cell: exosomes, microparticles and apoptotic bodies. While tumor-stroma interactions are in part mediated by the release of soluble factors such as growth factors, there is growing interest in the role of small membrane-bound vesicles in mediating such interactions. 1 These features indicate that gliomas extensively modulate their local environment to achieve successful invasive growth. They typically grow as widely infiltrative lesions, evade local innate immune surveillance, and induce proliferation of local vasculature.

Gliomas are the most common and deadly of adult primary brain tumors. Our data suggest that the scope of potential actions of tumor-derived microvesicles is much broader and more complex than previously supposed, and highlight a number of new classes of small RNA that remain to be characterized. Short-term exposure of brain microvascular endothelial cells to glioma microvesicles results in many gene expression changes in the endothelial cells, most of which cannot be explained by direct delivery of transcripts. Microvesicles show a relative depletion in microRNA compared with their cells of origin, and are enriched in unusual or novel noncoding RNAs, most of which have no known function.

We find that glioma microvesicles are predominantly of exosomal origin and contain complex populations of coding and noncoding RNAs in proportions that are distinct from those in the cells from which they are derived. Here we have taken an unbiased approach to identifying RNAs in glioma-derived microvesicles, and explored their potential to regulate gene expression in recipient cells. Communication with host cells and stroma via microvesicles represents one pathway by which tumors can modify their surroundings to achieve a tumor-permissive environment.

Interactions between glioma cells and their local environment are critical determinants of brain tumor growth, infiltration and neovascularisation.

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