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Journal of Oncology
Volume 2019, Article ID 1805841, 10 pages
https://doi.org/10.1155/2019/1805841
Research Article

The SR-B1 Receptor as a Potential Target for Treating Glioblastoma

1Lipoprotein Drug Delivery Laboratory, Department of Physiology/Anatomy, USA
2Neurosurgery, Presbyterian Hospital, Plano, TX, USA
3Department of Pediatrics, University of North Texas Health Science Center, Fort Worth, TX, USA

Correspondence should be addressed to Andras G. Lacko; ude.cshtnu@okcal.sardna

Received 25 February 2019; Revised 22 April 2019; Accepted 12 May 2019; Published 3 June 2019

Academic Editor: Akira Hara

Copyright © 2019 Ethan Berney et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Purpose. The goal of these studies was to provide proof of concept for a novel targeted therapy for Glioblastoma Multiforme (GBM). Methods. These studies involve the evaluation of reconstituted high density lipoprotein (rHDL) nanoparticles (NPs) as delivery agents for the drug, mammalian Target of Rapamycin (mTOR) inhibitor Everolimus (EVR) to GBM cells. Cytotoxicity studies and assessment of downstream effects, including apoptosis, migration, and cell cycle events, were probed, in relation to the expression of scavenger receptor B type 1 (SR-B1) by GBM cells. Results. Findings from cytotoxicity studies indicate that the rHDL/EVR formulation was 185 times more potent than free EVR against high SR-B1 expressing cell line (LN 229). Cell cycle analysis revealed that rHDL/EVR treated LN229 cells had a 5.8 times higher apoptotic cell population than those treated with EVR. The sensitivity of GBM cells to EVR treatment was strongly correlated with SR-B1 expression. Conclusions. These studies present strong proof of concept regarding the efficacy of delivering EVR and likely other agents, via a biocompatible transport system, targeted to the SR-B1 receptor that is upregulated in most cancers, including GBM. Targeting the SR-B1 receptor could thus lead to effective personalized therapy of GBM.