Targeting scavenger receptor B1 in pancreatic cancer by ApoA-II/rHDL nanoparticles — The Association Specialists
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Targeting scavenger receptor B1 in pancreatic cancer by ApoA-II/rHDL nanoparticles (260)

Sohel M Julovi 1 , Aiqun Xue 1 , Jaswinder S Samra 2 , Anthony J Gill 3 , Thomas J Hugh 2 , Jerikho Christian Yap Bulanadi 1 , Kerry-Anne Rye 4 , Minoo Moghaddam 5 , Ross C Smith 1
  1. Cancer Surgery Research Group, Kolling Institute of Medical Research, University of Sydney at RNSH, St Leonards, NSW, Australia
  2. Department of Gastrointestinal Surgery, Royal North Shore Hospital, St Leonards
  3. Deaprtment of Pathology, Royal North Shore Hospital, St Leonards
  4. Centre for Vascular Research, Faculty of Medicine, University of New South Wales
  5. CSIRO Materials Science & Engineering, North Ryde, Sydney

Background: Scavenger receptor class B type I (SR-BI) is a multi-ligand receptor that binds a variety of lipoproteins, including high density lipoprotein (HDL) and low density lipoprotein (LDL). Our recent study shows that recombinant (r) HDL using Apolipoprotein A-II (rHDL/ApoA-II) targets pancreatic ductal adenocarcinoma (PDAC) xenografts. This targeting of rHDL/ApoA-II may be due to its specific high-affinity to SR-B1 and that this could be utilized for the selective delivery of anticancer drugs to PDAC.
Aims: In this study we investigated whether SR-B1 is over expressed in pancreatic cancer (PC) cell lines and human PC compared to normal pancreatic cells and normal pancreatic tissue.
Methods: Immunoblotting was undertaken on normal human pancreatic ductal epithelial (HPDE6) cells and pancreatic cancer cell lines CFPAC-1. Immunohistochemistry (IHC) was performed on patient derived PDAC tissue, primary PDAC xenografts and normal pancreas. The rHDL uptake by patient derived xenograft tumour (PDXT) in NOD/SCID mice was assessed by Carestream molecular imaging (MI).
Results: The expression of SR-B1 was 4 fold and 3.7 fold greater in CFPAC-1 cancer cells and PDAC tissue respectively, compared to HPDE6 cells and normal pancreas. Exogenous rHDL uptake by PDXT was enhanced 3.4 fold by the addition of ApoA-II.
Conclusions: The increased expression of the SR-B1 receptor in pancreatic cancer may be the mechanism allowing increased uptake of rHDL/ApoA-II, this finding may have theranostic potentialities for pancreatic cancer.