Secretion of functionally active complement factor H related protein 5 (FHR5) by primary tumour cells derived from Glioblastoma Multiforme patients |
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| Authors: | Syreeta DeCordova Amr Abdelgany Valarmathy Murugaiah Ansar A. Pathan Annapurna Nayak Tom Walker Abhishek Shastri Salman H. Alrokayan Haseeb A. Khan Shiv K. Singh Nick De Pennington Robert B. Sim Uday Kishore |
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| Affiliation: | 1. Biosciences, College of Health and Life Sciences, Brunel University London, Uxbridge, UB8 3PH, UK;2. Nuffield Department of Clinical Neuroscience, John Radcliffe Hospital, University of Oxford, Headington, OX3 9DS, UK;3. Department of Oncology, University of Oxford, Roosevelt Drive, Oxford, OX3 7DQ, UK;4. Westminster Community Mental Health Team, Central and North-West London NHS Foundation Trust, London SW1V 1DX, UK;5. Department of Biochemistry, College of Science, King Saud University, Riyadh 11451, Saudi Arabia;6. Department of Gastroenterology and Gastrointestinal Oncology, University Medical Centre, Goettingen, Germany;7. Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK |
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| Abstract: | The complement system is an important humoral immune surveillance mechanism against tumours. However, many malignant tumours are resistant to complement mediated lysis. Here, we report secretion of complement factor H related protein 5 (FHR5) by primary tumour cells derived from Glioblastoma multiforme (GBM) patients. We investigated whether the secreted FHR5 exhibited functional activity similar to factor H, including inhibition of complement mediated lysis, acting as a co-factor for factor I mediated cleavage of C3b, and decay acceleration of C3 convertase. Immunoblotting analysis of primary GBM cells (B30, B31 and B33) supernatant showed the active secretion of FHR5, but not of Factor H. ELISA revealed that the secretion of soluble GBM-FHR5 by cultured GBM cells increased in a time-dependent manner. Primary GBM-FHR5 inhibited complement mediated lysis, possessed co-factor activity for factor I mediated cleavage and displayed decay acceleration of C3 convertase. In summary, we detected the secretion of FHR5 by primary GBM cells B30, B31 and B33. The results demonstrated that GBM-FHR5 shares biological function with FH as a mechanism primary GBM cells potentially use to resist complement mediated lysis. |
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| Keywords: | Corresponding author. FHR5 FH Glioblastoma and complement |
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