Crosstalk-induced loss of miR-126 promotes angiogenesis.

A molecular environment that promotes vascularization around human carcinomas can materialise rapidly, and has been termed the angiogenic switch. Turning this switch toward a proangiogenic state involves an altered interplay between tumor cells and multiple components of the surrounding stroma. The regulatory landscape of these interactions in cervical cancer is now investigated by Huang et al. in this issue of Oncogene, who demonstrate that the microRNA miR-126 is downregulated during cancer progression, particularly in stromal cells. Such a reduction of miR-126 is shown to free at least one target, the proangiogenic adrenomedullin, from repression, enhancing vascular growth especially at the in situ to invasive carcinoma transition. The study implicates the temporal, spatial and progressive nature of tumor-stroma interactions during carcinogenesis, while in turn suggesting therapeutic strategies.