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Genes encoding multiple forms of phospholipase A2 are expressed in immature forms of human leukemic blasts

Leukemia volume 23, pages 1196–1199 (2009)Cite this article

Phospholipase A2 (PLA2) catalyzes the hydrolysis of the sn-2 position of membrane glycerophospholipids to liberate the eicosanoid precursor, arachidonic acid (AA).1, 2 Three distinct families have been documented: low molecular weight soluble forms of PLA2 (sPLA2); Ca2+-dependent high molecular weight PLA2 (cPLA2) and Ca2+-independent high molecular weight PLA2 (iPLA2). The sPLA2 family is implicated in several biological processes such as inflammation and host defense.1, 2 Nine isoenzymes have been identified. Among them sPLA2-IB is the pancreatic one. sPLA2-IIA is constitutively expressed in various organs related to immune response such as bone marrow, spleen and thymus. sPLA2-V is found in several immune cells such as macrophage, mast cells and type II helper T cells. sPLA2-X is expressed in the digestive tract, immune organs and blood leukocytes. The cPLA2 family consisted of four members, cPLA2-IVA, cPLA2-IVB, cPLA2-IVC and cPLA2-IVD; cPLA2-IVA being the central regulator of stimulus-coupled cellular AA release.1, 2 The iPLA2 (PLA2-VI) plays a major role in phospholipids remodeling.

Eicosanoid products of the cyclooxygenase (COX) and lipoxygenase pathways of AA are important mediators of malignant proliferation.3 Deregulated PLA2 activity contributes to the pathogenesis of several malignancies including prostate cancer, ovarian carcinoma and colorectal adenocarcinoma.1, 2 The COX and lipoxygenase pathways of AA have been recently documented on immature leukemic blasts of patients with acute myeloid (AML) and acute lymphoid (ALL) leukemia.4, 5 Thus, freshly isolated AML and ALL blasts express COX-1, produce the AA metabolite prostaglandin E2, express functional EP2 receptors and increase their growth in response to exogenously added prostaglandin E2. The World Health Organization has proposed a classification system that divides AML into several broad groups: AML with genetic abnormalities, AML with multilineage dysplasia, AML related to earlier chemotherapy or radiation and AML not otherwise specified. The latter group contains a subgroup, AML without maturation, which consisted of the weaker immature blast group. In view of the potentially important oncogenic action of PLA2 in leukemic proliferation, quantitative PCR was used to determine the PLA2 mRNAs that were expressed in AML blasts without maturation and ALL blasts.

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Acknowledgements

This work was supported in part by a grant from ‘Le Lions Club de la Corrèze, Zone 33 District 103 Sud’.

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  1. Université de Limoges, Centre National de la Recherche Scientifique, Limoges, France

    R Fiancette, C Vincent, D Bordessoule & Y Denizot

  2. Laboratoire d’Hématologie, CHU Dupuytren, Limoges, France

    M Donnard & F Trimoreau

  3. Service d’Hématologie Clinique et de Thérapie Cellulaire, CHU Dupuytren, Limoges, France. E-mail: yves.denizot@unilim.fr,

    D Bordessoule & P Turlure

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Fiancette, R., Vincent, C., Donnard, M. et al. Genes encoding multiple forms of phospholipase A2 are expressed in immature forms of human leukemic blasts. Leukemia 23, 1196–1199 (2009). https://doi.org/10.1038/leu.2009.36

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