We previously reported that MX2, a new morpholino anthracycline, showed marked effects on pleiotropic drug-resistant sublines of murine P388 leukemia in vivo as well as in vitro. In this study we examine the in vitro cytotoxicity against pleiotropic drug-resistant sublines of human tumor cell lines. MX2 was effective against multidrug-resistant sublines of four human tumor cell lines; these cel...

Previously, we characterized a zinc finger protein gene HZF1 (ZNF16) and demonstrated that it played a significant role in the erythroid and megakaryocytic differentiation of K562 cells by knockdown of the gene. In this study, we examined the effect of HZF1 on the proliferation and apoptosis of K562 cells and identified the possible mechanism for this effect. By lentivirus-mediated gene transfe...

Resistance to imatinib is commonly associated with reactivation of Bcr-Abl signalling. However, Bcr-Abl-independent signalling pathways may be activated and contributed to imatinib resistance in some CML (chronic myelogenous leukaemia) patients. We had isolated three imatinib-resistant K562/R1, R2 and R3 variants with gradual loss of Bcr-Abl from K562 cells to develop effective therapeutic stra...

We have investigated the hormonal responsiveness of K562 cells using a serum-substituted in vitro clonogenic assay. Dexamethasone inhibited colony formation by the K562 cells. and the inhibitory effect could be reversed by progesterone (10 M). Fluoxymesterone caused a prominent enhancement of K562 colony growth. whereas estriol had no effect. Stimulation by triiodothyronine was maximal at iO M....

Asciminib (previously ABL001), which binds the myristate-binding pocket of the Bcr-Abl kinase domain, is in phase I clinical trials as monotherapy and in combination with imatinib, nilotinib and dasatinib for the treatment of patients with refractory CML or Ph+ ALL. Asciminib sensitivity was evaluated in asciminib naïve BCR-ABL1+ cell lines K562 (negligible ABCB1/ABCG2 expression), K562-Dox (AB...

We previously reported that natural killer (NK)-sensitive target cells, K562, kill interleukin-2-stimulated (lymphokine-activated killer [LAK]) but not unstimulated NK cells. We have now investigated the molecular basis of this phenomenon. Soluble monoclonal antibody (MoAb) to CD18 inhibited 75% of K562-induced DNA fragmentation and membrane disruption, whereas blocking MoAb to Fas partially in...

K562-R, a pleiotropic drug-resistant cell line established in vitro, and K562-S, the chemotherapy-sensitive parent line, were used as targets in the natural killer cell (NK) system. At each of the effector:target ratios studied, the K562-R demonstrated a decrease in their susceptibility to both unstimulated and interferon-activated NK cells, as compared to the K562-S line. This difference did n...

background: rna interference (rnai) is the mechanism of gene silencing-mediated messenger rna degradation by small interference rna (sirna), which becomes a powerful tool for in vivo research, especially in the areas of cancer. in this research, the potential use of an expression vector as a specific sirna producing tool for silencing of bcr-abl in k562 cell line has been investigated. methods:...