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Title: Enhanced expression of CD31/platelet endothelial cell adhesion molecule 1 (PECAM1) correlates with hypoxia inducible factor-1 alpha (HIF-1α) in human glioblastoma multiforme

Journal Article · · Experimental Cell Research
;  [1];  [2];  [3];  [1];  [4]
  1. Department of Biomedical and Biotechnological Sciences, Section of Human Anatomy and Histology, School of Medicine, University of Catania, 95123 Catania (Italy)
  2. Department G.F. Ingrassia, Azienda Ospedaliero-Universitaria “Policlinico-Vittorio Emanuele”, Section of Anatomic Pathology, University of Catania, Via S. Sofia 87, 95123 Catania (Italy)
  3. Department of Biomedical Sciences and Biotechnologies, Section of Physiology, University of Catania, Via S. Sofia 87, 95125 Catania (Italy)
  4. Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari, Medical School, Policlinico – Piazza G. Cesare, 11, 70124 Bari (Italy)

Glioblastoma multiforme (GBM) is characterized by numerous abnormal blood vessels, which rapidly proliferate and invade brain tissue and express different angiogenic factors. In this study we have investigated whether the expression levels of CD31/ PECAM1 are deregulated in human GBM tissue specimens and we have also correlated the expression levels of CD31/PECAM1 with those of HIF-1α. Finally, we have established a correlation between the expression levels of CD31/PECAM1 and HIF-1α, and those of two other biomarkers, namely N-cadherin and ADAM-10, of aggressiveness in the same tumors. Results have shown an increased expression of CD31/PECAM1 correlated to HIF-1α expression, confirming evidence demonstrating that different types of tumor are able to trigger aberrant angiogenesis through HIF-1α. Moreover, we also established a further correlation among CD31/PECAM1 and HIF-1α and N-cadherin and ADAM-10, two other markers of aggressiveness in the same tumors.

OSTI ID:
22746392
Journal Information:
Experimental Cell Research, Vol. 339, Issue 2; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
Country of Publication:
United States
Language:
English