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Your search keyword '"Wielockx, Ben"' showing total 10 results
Start Over Author "Wielockx, Ben" Publisher mdpi ag
10 results on '"Wielockx, Ben"'

2. Erythropoietin Receptor (EPOR) Signaling in the Osteoclast Lineage Contributes to EPO-Induced Bone Loss in Mice

Author

Awida, Zamzam, primary, Hiram-Bab, Sahar, additional, Bachar, Almog, additional, Saed, Hussam, additional, Zyc, Dan, additional, Gorodov, Anton, additional, Ben-Califa, Nathalie, additional, Omari, Sewar, additional, Omar, Jana, additional, Younis, Liana, additional, Iden, Jennifer Ana, additional, Graniewitz Visacovsky, Liad, additional, Gluzman, Ida, additional, Liron, Tamar, additional, Raphael-Mizrahi, Bitya, additional, Kolomansky, Albert, additional, Rauner, Martina, additional, Wielockx, Ben, additional, Gabet, Yankel, additional, and Neumann, Drorit, additional

Published
2022
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9. PHD3 Acts as Tumor Suppressor in Mouse Osteosarcoma and Influences Tumor Vascularization via PDGF-C Signaling

Author

Egners, Antje, Rezaei, Maryam, Kuzmanov, Aleksandar, Poitz, David M., Streichert, Doreen, Müller-Reichert, Thomas, Wielockx, Ben, and Breier, Georg

Subjects
prolyl hydroxylase domain protein, PDGF-C, tumor progression, tumor angiogenesis, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, PDGFR-α, lcsh:RC254-282, Article
Abstract

Cancer cell proliferation and insufficient blood supply can lead to the development of hypoxic areas in the tumor tissue. The adaptation to the hypoxic environment is mediated by a transcriptional complex called hypoxia-inducible factor (HIF). HIF protein levels are tightly controlled by oxygen-dependent prolyl hydroxylase domain proteins (PHDs). However, the precise roles of these enzymes in tumor progression and their downstream signaling pathways are not fully characterized. Here, we study PHD3 function in murine experimental osteosarcoma. Unexpectedly, PHD3 silencing in LM8 cells affects neither HIF-1&alpha, protein levels, nor the expression of various HIF-1 target genes. Subcutaneous injection of PHD3-silenced tumor cells accelerated tumor progression and was accompanied by dramatic phenotypic changes in the tumor vasculature. Blood vessels in advanced PHD3-silenced tumors were enlarged whereas their density was greatly reduced. Examination of the molecular pathways underlying these alterations revealed that platelet-derived growth factor (PDGF)-C signaling is activated in the vasculature of PHD3-deficient tumors. Silencing of PDGF-C depleted tumor growth, increased vessel density and reduced vessel size. Our data show that PHD3 controls tumor growth and vessel architecture in LM8 osteosarcoma by regulating the PDGF-C pathway, and support the hypothesis that different members of the PHD family exert unique functions in tumors.

Published
2018

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