Abstract
Smenospongine, a sesquiterpene aminoquinone isolated from the marine sponge Dactylospongia elegans, was previously reported by us to induce erythroid differentiation and G1 phase arrest of K562 chronic myelogenous leukemia cells. In this study, we investigated the effect of smenospongine on the cell cycles of other leukemia cells, including HL60 human acute promyelocytic leukemia cells and U937 human histiocytic lymphoma cells by flow cytometric analysis. Smenospongine induced apoptosis dosedependently in HL60 and U937 cells. The smenospongine treatment increased expression of p21 and inhibited phosphorylation of Rb in K562 cells, suggesting the p21-Rb pathway play an important role in G1 arrest in K562 cells. However, the p21 promoter was not activated by the smenospongine treatment based on a luciferase assay using the transfected K562 cells. Smenospongine might induce p21 expression via another mechanism than transactivation of p21 promoter.
Highlights
Chronic myelogenous leukemia (CML) is a hematopoietic stem cell cancer caused by the Bcr-Abl tyrosine kinase which arised from Philadelphia chromosome (Ph) translocation [1,2]
We recently investigated the effect of smenospongine on other leukemia cells such as HL60 and U937 by cell cycle analysis and further investigated the mechanism for the G1 arrest in
To investigate whether this compound has the same effect on other leukemia cells or not, cell cycle analysis for HL60 and U937 cells together with K562 cells was carried out
Summary
Chronic myelogenous leukemia (CML) is a hematopoietic stem cell cancer caused by the Bcr-Abl tyrosine kinase which arised from Philadelphia chromosome (Ph) translocation [1,2]. A selective inhibitor of Bcr-Abl, imatinib mesylate (Glivec®), was developed as the first molecule-targeted anticancer drug [4]. With the widespread use of this drug, the resistance in some patients has been well reported, which is usually caused by mutations within Bcr-Abl [3,5,6]. It was reported that FK228, a histone deacetylase (HDAC) inhibitor, was indicated to be therapeutically effective in treating CML, and AML (acute myelogenous leukemia) and lymphocytic leukemia [7,8,9]. Whether smenospongine shows the same effect on other leukemia cells or not, remained unclear. We recently investigated the effect of smenospongine on other leukemia cells such as HL60 and U937 by cell cycle analysis and further investigated the mechanism for the G1 arrest in
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