Search results

Search:
in the keywords: K562 cells

Sort By:

Limit search:

Inhibition of cell proliferation and induction of apoptosis in K562 human leukemia cells by the derivative (3-NpC) from dihydro-pyranochromenes family

100%

Rahimi R., Mahdavi M., Pejman S., Zare P., Balalaei S.

2015

vol. 62

issue 1

83-88

Leukemia is a particular type of cancer characterized by the failure of cell death or disability in differentiation of hematopoietic cells. Chronic myelogenus leukemia (CML) is the most studied kind of this cancer. In this study, anti-cancer effect of dihydro-pyranochromenes derivatives were investigated in the human leukemia K562 cells. These compounds were found to be active cell proliferation inhibitors using MTT assay. Among these compounds, 3-NpC was determined as stronger compound with IC50 value of 100±3.1 µM and was chosen for further studies. Induction of apoptosis was analyzed by AO/EtBr staining, DNA fragmentation assay, Annexin V/PI double staining and cell cycle analysis. Furthermore, Western Blot analysis showed that treatment of the cells with 3-NpC led to up-regulation and activation of caspase-3. The results of this investigation clearly indicated that dihydro-pyranochromenes derivatives induce apoptosis in the K562 cell line. This information signalizes also that these compounds may prepare a new therapeutic approach for the treatment of leukemia.

Hyperthermia can differentially modulate the repair of doxorubicin-damaged DNA in normal and cancer cells*.

100%

Blasiak J., Widera K., Pertyński T.

Hyperthermia can modulate the action of many anticancer drugs, and DNA repair processes are temperature-dependent, but the character of this dependence in cancer and normal cells is largely unknown. This subject seems to be worth studying, because hyperthermia can assist cancer therapy. A 1-h incubation at 37°C of normal human peripheral blood lymphocytes and human myelogenous leukemia cell line K562 with 0.5 μM doxorubicin gave significant level of DNA damage as assessed by the alkaline comet assay. The cells were then incubated in doxorubicin-free repair medium at 37°C or 41°C. The lymphocytes incubated at 37°C needed about 60 min to remove completely the damage to their DNA, whereas at 41°C the time required for complete repair was shortened to 30 min. There was also a difference between the repair kinetics at 37°C and 41°C in cancer cells. Moreover, the kinetics were different in doxorubicin-sensitive and resistant cells. Therefore, hyperthermia may significantly affect the kinetics of DNA repair in drug-treated cells, but the magnitude of the effect may be different in normal and cancer cells. These features may be exploited in cancer chemotherapy to increase the effectiveness of the treatment and reduce unwanted effects of anticancer drugs in normal cells and fight DNA repair-based drug resistance of cancer cells.

Combined effects of doxorubicin and STI571 on growth, differentiation and apoptosis of CML cell line K562

75%

Jakubowska J., Stasiak M., Szulawska A., Bednarek A., Czyz M.

2007

vol. 54

issue 4

839-846

STI571 (imatinib mesylate; Gleevec®) is an inhibitor that targets the tyrosine kinase activity of Bcr-Abl present in chronic myelogenous leukemia (CML) cells. Some preclinical studies have demonstrated that the combination of STI571 with chemotherapeutic drugs results in enhanced toxicity in Bcr-Abl-positive leukemias. We investigated the potential benefit of using STI571 to down-regulate Bcr-Abl activity for the enhancement of doxorubicin anti-proliferative action in K562 cell line derived from blast crisis of CML. At low concentrations of both drugs (40 nM doxorubicin combined with STI571 in the range of 100-150 nM), the antiproliferative effects were mainly due to cellular differentiation as assessed by benzidine staining for hemoglobin synthesis level and real-time PCR for γ-globin expression. Higher concentrations of STI571 used in combinations with doxorubicin caused mainly apoptosis as shown by DNA degradation and nuclear fragmentation visualized by fluorescence microscopy after DAPI staining, changes in cell morphology observed after Giemza-May Grünwald staining and cellular membrane organization estimated by flow cytometry after Annexin V staining. As compared with either drug alone, cotreatment with STI571 and DOX induced stronger cellular responses. A low concentration of STI571 in combination with a low concentration of DOX might be tested as an alternative approach to increasing the efficacy of chemotherapy against CML.

Refine search results

3 Acta Biochimica Polonica

1 2015

1 2007

1 2003

1 Balalaei S.

1 Bednarek A.

1 Blasiak J.

1 Czyz M.

1 Jakubowska J.

1 Mahdavi M.

1 Pejman S.

1 Pertyński T.

1 Rahimi R.

1 Stasiak M.

1 Szulawska A.

1 Widera K.

1 Zare P.

Search results

Inhibition of cell proliferation and induction of apoptosis in K562 human leukemia cells by the derivative (3-NpC) from dihydro-pyranochromenes family

Hyperthermia can differentially modulate the repair of doxorubicin-damaged DNA in normal and cancer cells*.

Combined effects of doxorubicin and STI571 on growth, differentiation and apoptosis of CML cell line K562