3-methoxyapigenin modulates β-catenin stability and inhibits Wnt/β-catenin signaling in Jurkat leukemic cells.

Aims: Aberrant activation of Wnt/β-catenin signaling has been implicated in carcinogenesis. Identification of inhibitors of this pathway may help in cancer therapy. The purpose of this study is to investigate the inhibitory effect of 3-methoxyapigenin (3-MA) with β-catenin/LEF reporter system.

Prevalence of MPL W515L/K mutations in Taiwanese patients with Philadelphia-negative chronic myeloproliferative neoplasms.

Background: The discovery of Janus kinase 2 (JAK2)-V617F has provided important insight into the pathogenesis of Philadelphia-negative chronic myeloproliferative neoplasms (Ph-negative MPNs); however, the etiology of JAK2(V617F)-negative Ph-negative MPN remains unidentified. MPL(W515L) and MPL(W515K) (MPL(W515L/K)) are 2 gain-of-function mutations, which have been found in some Ph-negative MPN patients from Western countries. However, little is known about the incidence of these mutations in Taiwanese Ph-negative MPN patients.

Blockade of JAK2 activity suppressed accumulation of β-catenin in leukemic cells.

The Wnt/β-catenin pathway has been implicated in leukemogenesis. We found β-catenin abnormally accumulated in both human acute T cell leukemia Jurkat cells and human erythroleukemia HEL cells. β-Catenin can be significantly down-regulated by the Janus kinase 2 specific inhibitor AG490 in these two cells.

Involvement of endoplasmic reticulum in paclitaxel-induced apoptosis.

The participation of the mitochondrial pathway in paclitaxel-induced apoptosis has been well documented. After addition of paclitaxel to U937 cells, however, we observed an early expression of five endoplasmic reticulum (ER) stress response genes that preceded the release of cytochrome c from the mitochondria and the cleavage of the caspases. Involvement of the ER was supported by the following evidence.

Cell cycle specific induction of apoptosis and necrosis by paclitaxel in the leukemic U937 cells.

Induction of cell apoptosis and necrosis by paclitaxel was investigated in human leukemic U937 cells. To explore whether paclitaxel induces both apoptosis and necrosis in different cell cycle stages, we synchronized the cells in G1, S and G2/M stages by counterflow centrifugal elutriation (CCE). The Annexin V and PI analysis revealed that, after paclitaxel treatment, the cells in G1 and S stages died predominantly through apoptosis, whereas G2/M-stage cells died through both apoptosis and necrosis.

Detection of bcr-abl gene expression at a low level in blood cells of some patients with essential thrombocythemia.

The major bcr-abl fusion gene is seen as a major marker of chronic myeloid leukemia (CML). However, whether the bcr-abl transcript can be detected in patients with essential thrombocythemia (ET) is still a matter of controversy. We detected the messenger RNA expression of the bcr-abl gene using reverse transcription-polymerase chain reaction in peripheral-blood leukocytes (PBLs) from 63 patients with myeloproliferative disorders (including CML, ET, and polycythemia vera [PV]) and 51 normal, healthy volunteers.

Synthesis and immunofluorescence assay of a new biotinylated paclitaxel.

7-(5'-Biotinylamidopropanoyl)paclitaxel was synthesised by chemical methods; its immunofluorescence assay and the cell uptake experiments were performed by use of human leukemia U937 cells. The results indicate that paclitaxel is arresting cell cycle at the G(2)M phase only.