European journal of pharmacology · 2020
Targeting SKP2/Bcr-Abl pathway with Diosmetin suppresses chronic myeloid leukemia proliferation.
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Liu Yuan, Shao Zhenlong, Liao Yuning, Xia Xiaohong, Huang Chuyi, He Jinchan, Hu Tumei, Yu Cuifu, Jiang Lili, Liu Jinbao, Huang Hongbiao
Аннотация
Bcr-Abl is the primary cause as well as currently key therapeutic target of chronic myeloid leukemia (CML). SKP2, an E3 ligase, is a downstream factor of Bcr-Abl to motivate the cell cycle transition of CML and also found to bind and activate Bcr-Abl in reverse. Therefore, SKP2/Bcr-Abl pathway is an attractive target for CML treatment. This study aims to identify an inhibitor of the SKP2/Bcr-Abl pathway based on a large screening of the natural products. We demonstrate that Diosmetin, a kind of phytoestrogens, notably downregulates the expression of SKP2, Bcr-Abl phosphorylation, and moderately downregulates the Bcr-Abl level. Furthermore, Diosmetin displays a favorable anti-tumor activity in CML cells and xenograft models. Collectively, our study reveals a natural compound in the treatment of CML on the basis of SKP2/Bcr-Abl signaling pathway.
Предметные рубрики MeSH
AnimalsAntineoplastic Agents, PhytogenicApoptosisCell ProliferationDown-RegulationDrug Resistance, NeoplasmFlavonoidsFusion Proteins, bcr-ablGene Expression Regulation, NeoplasticHumansImatinib MesylateK562 CellsLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMaleMice, Inbred BALB CMice, NudePhosphorylationProtein Kinase InhibitorsS-Phase Kinase-Associated ProteinsSignal TransductionTumor BurdenXenograft Model Antitumor Assays