title: CCL2/CCR2 signaling pathway in glioblastoma multiforme.
abstract: Glioblastoma multiform (GBM) is described as one of the most frequent primary brain tumors. These types of malignancies constitute only 15% of all primary brain tumors. Despite, extensive developments on effective therapeutic methods during the 20th century as well as the first decade of the present century (21st), the median survival rate for patients suffering from GBM is only approximately 15 months, even in response to multi-modal therapy. numerous types of reticuloendothelial system cells such as macrophages and microglial cells occupied within both GBM and also normal surrounding tissues. These immune cells acquire an otherwise activated phenotype with potent tumor-tropic functions that contribute to the glioma growth and invasion. The CC chemokine, CCL2 (previously named MCP-1) is of the most important CC chemokines family member involving in regulation of oriented migration and penetrative infiltration of mainly reticuloendothelial system cells specifically monocyte/macrophage phenotypes. Fundamental parts are played by CCL2 and its related receptor (the CCR2) in brain tumors and obviously in migration of monocytes from the bloodstream through the vascular endothelium. Therefore, CCL2/CCR2 axis is required for the routine immunological surveillance of tissues, in accordance with response to inflammation. Briefly, in this review, we have tried our best to collect the latest, straightened and summarize literature reports exist within data base regarding the interaction between microglia/macrophages and CCL2/CCR2 axis in GBM. We aimed to discuss potential application of this chemokine/receptor interaction axis for the expansion of future anti-glioma therapies as well.
authors.affiliation: Geriatric Care Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
authors.forename: Alireza
authors.initials: A
authors.lastname: Vakilian
authors.affiliation: Molecular Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
authors.forename: Hossein
authors.initials: H
authors.lastname: Khorramdelazad
authors.affiliation: Department of Hematology and Medical Laboratory Sciences, School of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran.
authors.forename: Parisa
authors.initials: P
authors.lastname: Heidari
authors.affiliation: Department of Hematology and Medical Laboratory Sciences, School of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran.
authors.forename: Zahra
authors.initials: Z
authors.lastname: Sheikh Rezaei
authors.affiliation: Molecular Medicine Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, Iran; Department of Hematology and Medical Laboratory Sciences, School of Allied Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran. Electronic address: ghassanshahi@gmail.com.
authors.forename: Gholamhossein
authors.initials: G
authors.lastname: Hassanshahi
mesh_terms: D000818:Animals; D001932:Brain Neoplasms / Q000188:drug therapy / Q000378:metabolism*; D018932:Chemokine CCL2 / Q000378:metabolism*; D005909:Glioblastoma / Q000378:metabolism*; D006801:Humans; D054390:Receptors, CCR2 / Q000378:metabolism*; D019707:Receptors, Chemokine / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*
chemical_list: C515334:CCR2 protein, human; D018932:Chemokine CCL2; D054390:Receptors, CCR2; D019707:Receptors, Chemokine
keywords: CC chemokine; CCL2; GBM; Glioblastoma; MCP-1