| Literature DB >> 29465264 |
Uri Rozovski1,2, David M Harris1, Ping Li1, Zhiming Liu1, Preetesh Jain1, Alessandra Ferrajoli1, Jan Burger1, Phillip Thompson1, Nitin Jain1, William Wierda1, Michael J Keating1, Zeev Estrov1.
Abstract
Unlike normal B-cells, and similar to fat cells, chronic lymphocytic leukemia (CLL) cells aberrantly express lipoprotein lipase (LPL), which contributes to free fatty acids (FFAs) metabolism. Here we show that, in CLL cells, the B-cell receptor (BCR) inhibitor ibrutinib reduced LPL mRNA and protein levels and inhibited FFA metabolism in vitro. Likewise, in CLL cells from ibrutinib-treated patients, FFA metabolism was reduced and eventually stopped. Because ibrutinib disrupts CLL cells' ability to use FFAs for energy production, and because various BCR-dependent cellular functions rely on a continuous supply of chemical energy, ibrutinib interrupts several pathways imperative for cellular function in CLL cells.Entities:
Keywords: CLL; ibrutinib; lipoprotein lipase; metabolism
Mesh:
Substances:
Year: 2018 PMID: 29465264 PMCID: PMC6135679 DOI: 10.1080/10428194.2018.1439167
Source DB: PubMed Journal: Leuk Lymphoma ISSN: 1026-8022