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Thrombospondin-1 is a matricellular protein with potent antitumour activities, the levels of whichdetermine the fate of many different tumours, including renal carcinomas. However, the factors thatregulate this protein remain unclear. In renal carcinomas, hypoxic conditions enhance the expression ofangiogenic factors that help adapt tumour cells to their hostile environment. Therefore, we hypothesizedthat anti-angiogenic factors should correspondingly be dampened. Indeed, we found that hypoxia decreasedthe thrombospondin-1 protein in several clear cell renal carcinoma cell lines (ccRCC), although notranscriptional regulation was observed. Furthermore, we proved that hypoxia stimulates multiple signalsthat independently contribute to diminish thrombospondin-1 in ccRCC, which include a decrease in theactivity of oxygen-dependent prolylhydroxylases (PHDs) and activation of the PI3K/Akt signalling pathway.In addition, thrombospondin-1 regulation in hypoxia proved to be important for ccRCC cell migration andinvasionThis work was supported by the Ministerio de Ciencia e Innovacion (MCINN)SAF2009-11113 and METOXIA, a Collaborative Project under the 7th ResearchFramework Programme of the European Union FP7-HEALTH-2007B (ref.HEALTH-F2-2009-222741

Autocrine stimulation of clear-cell renal carcinoma cell migration in hypoxia via HIF-independent suppression of thrombospondin-1