Emulsion de scott target9/14/2023 ![]() ![]() ![]() If lipid is the main source of energy for pancreatic cancer tissue it is possible that HDL is an important source of this lipid. Interestingly pancreatic cancer does not accumulate fludeoxyglucose (FDG) strongly enough to be reliable as a contrast agent for Positron Emission Tomography (PET) which probably indicates that pancreatic cancer has a preference for lipid as its main calorie source. Cancer cells have an increased expression of SR-B1in relation to the expression on their non-malignant cells of origin and it is possible that this results in increased uptake of HDL by the cancer tissue which is an explanation for the reduction in serum ApoA-II in PDAC cases. ApoA-II alters binding of HDL to SR-B1 in different tissues and is particularly attracted to steroidogenic tissue where the cholesterol is utilized for hormone synthesis but rapidly growing cancer cells also require cholesterol for cell membranes. These results in a relatively longer circulation time for HDL/ApoA-II. In addition, ApoA-II maintains HDL levels in part by inhibition of hepatic lipase. Thirty percent of HDL is associated with ApoA-II which is thought to make the HDL smaller than that with ApoA-I alone and makes the HDL/ApoA-II less attracted to the hepatic SR-B1. The lipoprotein on the surface of HDL binds to SR-B1and delivers its lipid into the cell through a pore formed by SR-B1 increasing the uptake of HDL-cholesteryl ester (CE), an essential nutrient for malignant cell proliferation and metastasis. ![]() SR-B1 is a multi-ligand receptor and highly expressed in a variety of tumor cells including prostate, breast, colorectal and ovarian cancer cells. The scavenger receptor class B type-1 (SR-B1) is prevalent in hepatocytes and attracts HDL where the lipid is endocytosed or diffused in hepatocytes. The most important role for HDL is the delivery of cholesterol from peripheral tissues to the liver where it is metabolised into bile salts or excreted to the bile. ApoA-II is a component of high density lipoprotein (HDL) where it has an important role in directing the fate of the metabolism of the lipid in the HDL. This work has been confirmed by Honda and colleagues and others. Serum apolipoprotein A-II (ApoA-II) was found to be depressed in pancreatic cancer patients and was a potential diagnostic biomarker. Commercial affiliation of the authors at CSIRO did not play any role in the study and did not have any competing interests relating to employment, consultancy, patents, products in development and marketed products. Commercial affiliation of the authors at CSIRO did not play any role in the study and did not have any competing interests relating to employment, consultancy, patents, products in development and marketed products.Ĭompeting interests: The authors have no conflict of interests. The study was supported by the CanSur foundation and partly by the Ramsay Research Teaching Fund but did not have any role in the study design, data collection and analysis, decision to publish or preparation of the manuscript. This study has not been published elsewhere or is not under consideration for a publication. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: All relevant data are within the paper and its Supporting Information fileįunding: Part of this study was presented and awarded as best poster at New Horizons 2014 and the Scientific Research Meeting, 17th-19th November, 2014. Received: SeptemAccepted: FebruPublished: March 22, 2016Ĭopyright: © 2016 Julovi et al. PLoS ONE 11(3):Įditor: Yingmei Feng, Beijing Key Laboratory of Diabetes Prevention and Research, CHINA (2016) Apolipoprotein A-II Plus Lipid Emulsion Enhance Cell Growth via SR-B1 and Target Pancreatic Cancer In Vitro and In Vivo. Citation: Julovi SM, Xue A, Thanh LE TN, Gill AJ, Bulanadi JC, Patel M, et al. ![]()
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