ArticleInternational journal of hematology2011
MK886 inhibits the proliferation of HL-60 leukemia cells by suppressing the expression of mPGES-1 and reducing prostaglandin E2 synthesis.
Article in International journal of hematology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Growth of T-cell lymphoma cells is inhibited by mPGES-1/PGE2 suppression via JAK/STAT, TGF-β/Smad3 and PI3K/AKT signal pathways.Translational cancer research · 2022Article
- A Role for Lipid Mediators in Acute Myeloid Leukemia.International journal of molecular sciences · 2019Review
- An ARC-Regulated IL1β/Cox-2/PGE2/β-Catenin/ARC Circuit Controls Leukemia-Microenvironment Interactions and Confers Drug Resistance in AML.Cancer research · 2019Article
- Regulation of mPGES-1 composition and cell growth via the MAPK signaling pathway in jurkat cells.Experimental and therapeutic medicine · 2018Article
- KPT-330 inhibition of chromosome region maintenance 1 is cytotoxic and sensitizes chronic myeloid leukemia to Imatinib.Cell death discovery · 2018Article
- Isolation of Petrocidin A, a New Cytotoxic Cyclic Dipeptide from the Marine Sponge-Derived Bacterium Streptomyces sp. SBT348.Marine drugs · 2017Article
- Neutrophil elastase and its therapeutic effect on leukemia cells.Molecular medicine reports · 2015Article
- Revealing the macromolecular targets of complex natural products.Nature chemistry · 2014Article
- Multifaceted roles of PGE2 in inflammation and cancer.Seminars in immunopathology · 2013Review
- Leukotriene biosynthesis inhibitor MK886 impedes DNA polymerase activity.Chemical research in toxicology · 2013Article
- Effect of GINS2 on proliferation and apoptosis in leukemic cell line.International journal of medical sciences · 2013Article
- mPGES-1 in leukemic cells of AML patients.International journal of hematology · 2012Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microsomal prostaglandin E synthase-1 (mPGES-1), an inducible enzyme that specifically catalyzes the conversion of prostaglandin H2 (PGH2) to prostaglandin E2 (PGE2), has been reported to be over-expressed in a variety of solid tumor cells and tissues, but not in normal tissues. Its association with leukemia, however, has not been fully investigated. Our study revealed, for the first time, that mPGES-1 is over-expressed in human acute myeloid leukemia HL-60 cells. Cytotoxicity assays and flow cytometry showed that MK886, an inhibitor of mPGES-1, inhibits proliferation of HL-60 cells and induces apoptosis in a dose- and time-dependent manner, which may result from down-regulation of mPGES-1 expression and PGE2 synthesis. Evaluation of mediators of apoptotic signaling revealed up-regulation of BAX expression and caspase-3 activity, as well as significant decreases in Bcl2 and P-Akt. We conclude that MK886 reduces the viability of leukemia HL-60 cells by reducing mPGES-1 expression and PGE2 synthesis in a dose-dependent manner, which strongly suggests that mPGES-1 inhibitors should be considered as promising candidates for leukemia treatment.
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