Abstract
In chronic lymphocytic leukaemia (CLL), lipoprotein lipase (LPL) mRNA overexpression is an established poor prognostic marker, its function, however, is poorly understood. Measuring extracellular LPL enzymatic activity and protein, we found no difference between levels in CLL patients and those of controls, both before and after heparin treatment in vivo and in vitro. Investigating LPL knock down effects, we determined five potential downstream targets, of which one gene, STXBP3, reportedly is involved in fatty acid metabolism. While possibly reflecting an epigenetic switch towards an incorrect transcriptional program, LPL overexpression by itself does not appear to significantly influence CLL cell survival.
Copyright © 2013 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Biomarkers, Tumor* / blood
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Biomarkers, Tumor* / genetics
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Cell Survival / drug effects
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Cell Survival / genetics
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Cells, Cultured
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Cohort Studies
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Gene Expression Profiling
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Gene Expression Regulation, Leukemic / drug effects
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Gene Knockdown Techniques
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HeLa Cells
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Humans
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Leukemia, Lymphocytic, Chronic, B-Cell / blood
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Leukemia, Lymphocytic, Chronic, B-Cell / diagnosis*
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Leukemia, Lymphocytic, Chronic, B-Cell / genetics
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Leukemia, Lymphocytic, Chronic, B-Cell / pathology
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Lipoprotein Lipase / antagonists & inhibitors
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Lipoprotein Lipase / blood
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Lipoprotein Lipase / genetics
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Lipoprotein Lipase / physiology*
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Microarray Analysis
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Predictive Value of Tests
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Prognosis
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RNA, Small Interfering / pharmacology
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Retrospective Studies
Substances
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Biomarkers, Tumor
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RNA, Small Interfering
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Lipoprotein Lipase