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

Rahimi, Roya; Mahdavi, Majid; Pejman, Sina; Zare, Payman; Balalaei, Saeed

doi:10.18388/abp.2014_825

Cited by 23 publications

(16 citation statements)

References 25 publications

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“…4B, 5). These data suggested that the breakdown of DNA that resulted in cell killing could be due to the cell cycle arrest and apoptosis induction (Rahimi et al, 2015;Dehkordi et al, 2015). These findings correspond with recent studies that showed the cytotoxicity and apoptosis inducing effects of different types of pyrano-pyridines on various types of cancer cells, such as human liver cancer cells, human cervical cancer cells and Human Tcell leukemia cells (Magedov et al, 2007;Magedov et al, 2008;Hassan et al, 2013).…”

Section: Discussionsupporting

confidence: 89%

Cytotoxic and apoptosis inducing effect of some pyrano [3, 2-c] pyridine derivatives against MCF-7 Breast Cancer Cells

et al. 2018

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Anti-cancer activities of some pyrano-pyridines have been previously reported. Herein, we investigated anti-proliferative and apoptotic effects of the novel pyrano [3, 2-c] pyridine (P.P, TPM.P, 4-CP.P and 3-NP.P) compounds against MCF-7 breast cancer cells. The MCF-7 cells were cultured in the presence of various concentrations (20-200 μM) of the tested compounds for 3 days and the cell viability was determined by MTT assay. Induction of apoptosis was qualitatively assayed by acridine orange/ethidium bromide (AO/EtBr) staining, DNA fragmentation assay, as well as quantitatively by Annexin V/PI double staining and cell cycle analysis. These compounds inhibited growth and proliferation of the MCF-7 cells in a dose- and time-dependent manner. The IC50 values of P.P, TPM.P, 4-CP.P and 3-NP.P after 24 h of exposure were calculated to be 100±5.0, 180±6.0, 60±4.0 and 140±5.0 μM, respectively. 4-CP.P was determined as the most potent compound and was chosen for further studies. The result of flow cytometric cell cycle analysis indicated an increase in sub-G1 population after 72 h treatment of the cells. Furthermore, this was accompanied by exposure of phosphatidylserine (PS) in the outer cell membrane after time course of treatment with the 4-CP.P. Based on these observations, the pyrano [3, 2-c] pyridines can be regarded as a valuable candidate for further pharmaceutical evaluations.

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Section: Discussionsupporting

confidence: 89%

Cytotoxic and apoptosis inducing effect of some pyrano [3, 2-c] pyridine derivatives against MCF-7 Breast Cancer Cells

et al. 2018

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“…Late apoptotic cells will also incorporate ethidium bromide and therefore stain orange, but, in contrast to necrotic cells, the late apoptotic cells will show condensed and often fragmented nuclei. Necrotic cells stain orange, but have a nuclear morphology resembling that of viable cells, with no condensed chromatin (5).…”

Section: Methodsmentioning

confidence: 99%

“…Apoptosis is a type of cell death used by multicellular organisms to prevent uncontrolled proliferation and to dispose of unwanted cells. Apoptosis is originally characterized by morphological changes, including membrane blebbing, DNA fragmentation, chromatin condensation, nuclear fragmentation, cell shrinkage and apoptotic body formation (5). Resistance to apoptosis is a reason for concern in developing effective chemotherapeutic agents in various types of cancer.…”

Section: Introductionmentioning

confidence: 99%

Induction of apoptosis and erythroid differentiation of human chronic myelogenous leukemia K562 cells by low concentrations of lidamycin

Zhang

Guo

et al. 2018

Oncol Rep

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Apoptosis induction and differentiation of promyelocytic leukemic cells into mature cells are major strategies for the drug-based treatment of leukemia. Lidamycin (LDM) which is a member of the enediyne antibiotic family exhibits extreme cytotoxicity. In the present study, the induction of apoptosis and differentiation in human chronic myeloid leukemia K562 cells by low concentrations of lidamycin were investigated. K562 cells were treated with lidamycin at various concentrations for 48 h, and accumulated in the metaphase as determined in previous experiments. Cell viability was determined using a Cell Counting Kit-8 (CCK-8) assay and the IC 50 value of lidamycin was 0.1±3.2 nM. Induction of apoptosis was investigated morphologically by acridine orange/ethidium bromide (AO/EtBr) staining. Growth inhibition and apoptosis induction were observed in cells treated with low concentrations of lidamycin. In addition, western blot analysis revealed that treatment of the K562 cells with lidamycin at low concentrations upregulated the expression of caspase-8 and caspase-3. The induction of differentiation in human chronic myeloid leukemia K562 cells by lidamycin at low concentrations was also investigated. The nitroblue tetrazolium reduction ability of K562 cells was increased following treatment with lidamycin. Low concentrations of lidamycin triggered erythroid differentiation among K562 cells, indicated by morphological changes, increased hemoglobin content, and the expression of cell surface antigens such as CD71. Additionally the expression of GATA-binding factor 1 (GATA-1) protein in low concentration lidamycin-treated K562 cells was increased. The results of the present study suggest that a low-concentration lidamycin exerts effects on apoptosis and erythroid differentiation induction by increasing the expression of caspases and GATA-1 protein. Lidamycin may serve a positive role in relevant targeted chemotherapy and may represent a potential candidate for chronic myelogenous leukemia differentiation-inducing treatment.

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“…K562 cell growth and viability were detected by MTT assay according to the literature [ 10 ]. Cells were seeded in 12-well plates at a density of 8×10 5 cells/well and incubated for 72 h at 37°C.…”

Section: Methodsmentioning

confidence: 99%

MiR-29 Induces K562 Cell Apoptosis by Down-Regulating FoxM1

et al. 2015

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BackgroundLeukemia seriously threatens human life and health. MicroRNAs can regulate cell growth, proliferation, and death. This article investigated the role of miR-29 on regulating leukemia cell growth, proliferation, and apoptosis.Material/MethodsmiR-29 and scramble miRNA were transfected to K562 cells. MTT assay, colony formation assay, caspase-3 activity detection, and flow cytometry were applied to test miR-29 effect on cell growth, proliferation, and apoptosis. Western blot was used to detect Forkhead box protein M1 (FoxM1) protein expression. After we transfected miR-29, K562 cells were transfected with FoxM1 siRNA to test cell apoptosis.ResultsK562 cell growth and proliferation were inhibited after transfection with miR-29. Apoptosis phenome and caspase-3 activation were observed. FoxM1 level decreased. SiRNA FoxM1 enhanced miR-29-induced K562 cell apoptosis. FoxM1 overexpression suppressed miR-26-induced K562 cell apoptosis.ConclusionsMiR-29 restrained K562 cell growth and proliferation. MiR-29 induced K562 cell apoptosis through down-regulating FoxM1.

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

Cited by 23 publications

References 25 publications

Cytotoxic and apoptosis inducing effect of some pyrano [3, 2-c] pyridine derivatives against MCF-7 Breast Cancer Cells

Cytotoxic and apoptosis inducing effect of some pyrano [3, 2-c] pyridine derivatives against MCF-7 Breast Cancer Cells

Induction of apoptosis and erythroid differentiation of human chronic myelogenous leukemia K562 cells by low concentrations of lidamycin

MiR-29 Induces K562 Cell Apoptosis by Down-Regulating FoxM1

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