In the present work, for the first time, employing in vitro co-culture study models we demonstrated the usefulness of AsA against the pro-angiogenic effects of gliomas. Tumor PI-103 manufacturer microenvironment refers to complex cellular and extracellular components surrounding tumor cells at each stage of carcinogenesis . Endothelial cell represent one of the critical cellular elements in the tumor microenvironment that plays a crucial role in the growth and progression of cancer through controlling angiogenesis . Recent literature suggests that anti-angiogenic strategy targeting endothelial cells in the tumor microenvironment could be important as endothelial cells are generally non-transformed and are considered less prone to acquire drug resistance . Therefore, use of nontoxic agents that could effectively target endothelial cells as well as the resultant pathological angiogenesis in the tumor microenvironment could be important in the prevention as well as treatment of cancers. In the present study, AsA treatment strongly inhibited the growth, tube formation as well as invasion/migration in endothelial cells, thereby highlighting its importance as a novel anti-angiogenic agent. Cell survival is maintained by a delicate balance between antiapoptotic and pro-apoptotic stimuli. Results from the present study showed that AsA treatment increases the expression of proapoptotic molecules while decreasing the expression of pro-survival and anti-apoptotic molecules such as phosphorylated Akt and survivin. Even though the present study was not designed to understand the sequence of signaling events in endothelial cells following AsA treatment, earlier studies have shown that serine/threonine kinase Akt phosphorylates and prevents the pro-apoptotic action of Bad . Furthermore, the role of Akt has been reported in caspases inactivation both directly through phosphorylating caspases and indirectly through promoting the expression of anti-apoptotic molecules such as survivin . More definite studies are still required to understand the mechanism/s underlying AsA-induced apoptosis in endothelial cells. A large number of pro- and anti-angiogenic cellular factors regulate angiogenesis in gliomas. Among them, VEGF has been implicated as a major paracrine mediator in the pathogenesis of gliomas and it has been shown to directly U0126 MEK inhibitor contribute to angiogenesis and blood brain barrier breakdown .