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Dabral, Swati; Muecke, Christian; Valasarajan, Chanil; Schmoranzer, Mario; Wietelmann, Astrid; Semenza, Gregg L; Meister, Michael; Muley, Thomas; Seeger-Nukpezah, Tamina; Samakovlis, Christos; Weissmann, Norbert; Grimminger, Friedrich; Seeger, Werner; Savai, Rajkumar; Pullamsetti, Soni S
Nature communications, 05/2019, Letnik: 10, Številka: 1Journal Article
Hypoxia signaling plays a major role in non-malignant and malignant hyperproliferative diseases. Pulmonary hypertension (PH), a hypoxia-driven vascular disease, is characterized by a glycolytic switch similar to the Warburg effect in cancer. Ras association domain family 1A (RASSF1A) is a scaffold protein that acts as a tumour suppressor. Here we show that hypoxia promotes stabilization of RASSF1A through NOX-1- and protein kinase C- dependent phosphorylation. In parallel, hypoxia inducible factor-1 α (HIF-1α) activates RASSF1A transcription via HIF-binding sites in the RASSF1A promoter region. Vice versa, RASSF1A binds to HIF-1α, blocks its prolyl-hydroxylation and proteasomal degradation, and thus enhances the activation of the glycolytic switch. We find that this mechanism operates in experimental hypoxia-induced PH, which is blocked in RASSF1A knockout mice, in human primary PH vascular cells, and in a subset of human lung cancer cells. We conclude that RASSF1A-HIF-1α forms a feedforward loop driving hypoxia signaling in PH and cancer.
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