Cytotoxicity in vitro, cell migration and apoptotic mechanism studies induced by ruthenium(ii) complexes

RSC Advances ◽  
2015 ◽  
Vol 5 (31) ◽  
pp. 24534-24543 ◽  
Author(s):  
Wei Li ◽  
Bing-Jie Han ◽  
Jun-Hua Yao ◽  
Guang-Bin Jiang ◽  
Yun-Jun Liu
Keyword(s):  
Cell Cycle ◽  
Cell Migration ◽  
Membrane Potential ◽  
Comet Assay ◽  
Cell Cycle Arrest ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Cycle Arrest ◽  
Apoptotic Mechanism

Four Ru(ii) complexes [Ru(N–N)2(DHBT)](ClO4)2 were synthesized and characterized. The cytotoxicity in vitro, apoptosis, comet assay, cell migration, ROS, mitochondrial membrane potential, cell cycle arrest and expression of proteins were investigated.

Evaluation of anticancer activity in vitro and in vivo of iridium(iii) polypyridyl complexes

2019 ◽  
Vol 43 (22) ◽  
pp. 8566-8579 ◽  
Author(s):  
Miao He ◽  
Qiao-Yan Yi ◽  
Wen-Yao Zhang ◽  
Lan Bai ◽  
Fan Du ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Membrane Potential ◽  
Cytotoxic Activity ◽  
Anticancer Activity ◽  
Cell Cycle Arrest ◽  
Mitochondrial Membrane ◽  
Polypyridyl Complexes ◽  
Cycle Arrest

Three new iridium(iii) polypyridyl complexes were synthesized. The cytotoxic activity in vitro and in vivo, apoptosis, cell cycle arrest, mitochondrial membrane potential, ROS and the expression of Bcl-2 family proteins were investigated.

Tet-Regulated Expression of Mutant Neutrophil Elastase in HL-60 Cells: A Cellular Model of Severe Congenital Neutropenia.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 1452-1452
Author(s):  
Andrew A.G. Aprikyan ◽  
Nara A. Markosyan
Keyword(s):  
Cell Cycle ◽  
Membrane Potential ◽  
Cell Cycle Arrest ◽  
Mitochondrial Membrane Potential ◽  
Neutrophil Elastase ◽  
Mitochondrial Membrane ◽  
Apoptotic Cell ◽  
Induced Expression ◽  
Maturation Arrest ◽  
Cycle Arrest

Abstract Severe congenital neutropenia (SCN) is an inheritable hematopoietic disorder characterized by extremely low level of circulating neutrophils, ineffective intramedulary hematopoiesis with “maturation arrest” at the promyelocytic stage of differentiation, recurrent severe infections, and evolution to acute myelogenous leukemia (AML). Accelerated apoptosis of bone marrow-derived myeloid progenitor cells and cell cycle arrest of CD34+ cells was reported in SCN patients. We also reported that heterozygous mutations in the neutrophil elastase (NE) gene have been identified in approximately 80% of SCN patients. Transient expression of mutant but not normal NE triggered accelerated apoptotic cell death of human promyelocytic HL-60 cells supporting the causative role of mutant NE in pathogenesis of SCN. Here we present cellular model of SCN based on newly established tet-off HL-60 human promyelocytic cell line with inducible doxycycline-regulated expression of mutant NE with 8-amino acid deletion identified in a patient evolved to develop AML. Induced expression of mutant elastase in tet-off HL-60 cells treated with DMSO led to a block of differentiation or “maturation arrest” at the promyelocytic stage of differentiation with a significantly reduced proportion of differentiated cells (approximately 20% vs 70% in control) and higher proportion (~40%) of primitive undifferentiated cells compared with control DMSO-treated HL-60 cells expressing only normal NE (~10%). Flow cytometry analysis of annexin V-labeled cells repeatedly revealed approximately 2-fold higher rate of apoptosis in tet-off HL-60 cells with induced expression of mutant NE compared with control cells. FACS analysis of DAPI-labeled tet-off HL-60 cells with induced expression of mutant NE revealed abnormal cell cycle progression with gradual accumulation and apparent arrest of cells in G1-phase of the cell cycle similar to that reported for SCN patients. Interestingly, the apoptotic cell shrinking and swelling as determined by flow cytometry was observed in all phases of the cell cycle suggesting that accelerated apoptosis rather than cell cycle arrest is the primary abnormality caused by expression of mutant NE, and the abnormal cell cycle progression is a consequence of this impaired cell survival. Further analysis revealed a dramatic reduction in mitochondrial membrane potential of tet-off HL-60 cells expressing mutant NE compared with control cells. The reduced mitochondrial membrane potential as determined by FACS was observed as early as 24 hours of induction of mutant NE expression and before the accelerated apoptosis or cell cycle arrest was detected. Western blot analysis demonstrated that caspase-3 was not activated in the cells even after 3 days of mutant NE induction. Further analysis of apoptosis regulators revealed a down-regulation of Bcl-2 expression and up-regulation of Bax in cells with induced expression of mutant elastase. These data suggest that mutant elastase-mediated “maturation arrest” of human promyelocytic cells in patients with SCN and SCN/AML is associated with reduced expression of anti-apoptotic Bcl-2 and upregulation of pro-apoptotic Bax proteins that trigger a dramatic reduction in mitochondrial membrane potential and subsequent caspase-independent apoptosis and cell cycle arrest. Current studies focused on elucidating and characterizing specific molecular interactions mediating the pro-apoptotic effect of mutant neutrophil elastase in SCN.

scholarly journals Methanolic extract of Moringa oleifera leaves induces Cell cycle arrest and downregulates Mitochondrial membrane potential in Dalton's Lymphoma cells.

2021 ◽  
Author(s):  
Sandeep Kumar ◽  
Alok Shukla ◽  
Praveen Kumar Verma ◽  
Rishi kant Singh ◽  
Naveen Kumar ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Membrane Potential ◽  
Side Effects ◽  
Cell Cycle Arrest ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Leaf Extract ◽  
Cycle Arrest ◽  
Dalton’S Lymphoma ◽  
Dalton's Lymphoma

Abstract Cancer is a group of diseases characterised by abnormal and undifferentiated cell growth that has the potential to spread to other parts of the body. It is the world's second leading cause of death and morbidity. According to the GLOBOCAN 2020 report, out of 19.3 million new cancer cases and 10 million deaths reported, 544352 new cases and 259793 deaths occurred by non-Hodgkin lymphoma (NHLs). Although, numerous therapeutic approaches like, surgery, radiotherapy, chemotherapy and immunotherapy have been developed to treat cancer, limited success has been achieved, possibly due to severe side effects associated with the drugs used during chemotherapy. Therefore, deciphering the novel compound with least side effects and highly potent against cancer is urgently required. In the present study we used leaf extract of M. oleifera, well-known for its anti-cancer efficacy against different cancer cells, however, its effect on Dalton’s lymphoma, a type of spontaneously occurring T cell lymphoma originated in the thymus of DBA mice is seriously lacking. Therefore, present study was aimed to analyze the therapeutic efficacy of M. oleifera against DL cells. Our results show that leaf extract of M. oleifera (MOML) significantly induces morphological changes in DL cells followed by chromatin condensation, nuclear fragmentation, and ROS generation. We also found significant changes in mitochondrial membrane potential (ΔΨm) in a dose dependent manner. Furthermore, apoptosis of DL cells induced by cell cycle arrest at G2/M and S phase suggested that MOML could be used to treat NHL effectively

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