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Assessment of Airway Smooth Muscle Growth and Division: In Vitro Studies
Published in Alastair G. Stewart, AIRWAY WALL REMODELLING in ASTHMA, 2020
DNA synthesis measured by flow cytometry is based upon the principle that cells in different stages of the cell cycle have different but predictable amounts of DNA.64,65 By the use of fluorochromes (e.g., propidium iodide, ethidium bromide, and acridine orange) as nuclear dyes which stoichiometrically bind to DNA, it is possible to distinguish in a single parameter three compartments of the cell cycle based solely on DNA content of exponentially dividing cells. These are the G0/G1, phase with diploid amounts of DNA, G2 and mitosis with tetraploid quantities of DNA, and S phase with variable intermediate amounts of DNA. A typical DNA distribution of exponentially growing smooth muscle cells is illustrated in Figure 3. Examples of typical DNA distribution profiles at different phases of the cell cycle are shown in Figure 2. A more detailed account of the application of flow cytometry to cell cycle analysis is described elsewhere.65–67 Clearly, flow cytometry is a very powerful tool which combines detection of DNA synthesis and immunocytochemical markers to provide indices of cell counting, ploidy, and the DNA content in cells.
Cytotoxic Phenanthridone Alkaloid Constituents of the Amaryllidaceae
Published in Spyridon E. Kintzios, Maria G. Barberaki, Evangelia A. Flampouri, Plants That Fight Cancer, 2019
Jerald J. Nair, Johannes van Staden
Pancratistatin together with two of its ester analogs (20, 22) at concentrations less than 1 µM exhibited strong cytostatic activity in 3Y1 rat embryo fibroblasts (Mutsuga et al. 2002). Cell cycle analysis showed that when cells were arrested at the G0/G1 phase via serum deprivation, progression to the S phase was hindered by all three compounds (Mutsuga et al. 2002). Furthermore, cells synchronized at the late G1/early S phase by hydroxyurea treatment were blocked in progressing through the S phase by compound 20, whilst compound 22 and pancratistatin did not affect cell cycle progress but in fact retarded it (Mutsuga et al. 2002). When the effects of 20 and 22 were evaluated in promyelocytic HL-60RG leukemia cells synchronized at the G0/G1 phase, the cells accumulated in the sub G0/G1 phase without progress to the S phase, indicative of apoptotic cells (Mutsuga et al. 2002).
Site-Selective cAMP Analogs in the Arrest of Cancer Cell Growth
Published in Robert I. Glazer, Developments in Cancer Chemotherapy, 2019
The cell cycle analysis was performed to examine whether the reduced cell proliferation observed in the cancer cell lines after treatment with the analogs was due to a specific block in one phase of the cell cycle. It was found that the fractions of breast and colon cancer cells in G1, S, and G2/M phases were not appreciably different between the control cells (untreated) and the cells treated with the analogs. Thus, the inhibition of cell growth induced by the cAMP analogs was not associated with a specific block in one phase of the cell cycle, confirming a previous report41 on cAMP-induced inhibition of human breast cancer cell lines. In contrast, 8-Cl-adenosine-treated cells exhibited a G1 block of cell cycle, indicating that the growth-inhibitory effect of 8-Cl-cAMP was not due to the cytotoxic effects of its adenosine metabolite.
Synthesis and biological evaluation of halogenated phenoxychalcones and their corresponding pyrazolines as cytotoxic agents in human breast cancer
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2022
Peter A. Halim, Rasha A. Hassan, Khaled O. Mohamed, Soha O. Hassanin, Mona G. Khalil, Amr M. Abdou, Eman O. Osman
Anticancer agents exert their cytotoxic action by terminating cellular proliferation at definite checkpoints found at different stages of the cell cycle. Suppression of these phases results in the termination of the cell proliferation. Cell cycle analysis employs flow cytometry to differentiate between cells within different phases of the cell cycle. In this work, the effect of the most active compound 2c on cell cycle progression was studied to explore the definite phase at which cell cycle arrest takes place in the MCF-7 breast cancer cell line. MCF-7 cells were treated with compound 2c at its IC50 concentration (1.52 μM) and its effect on the cell population in different cell phases was recorded and displayed in Figure 5. Exposure of MCF-7 cells to compound 2c resulted in significant decline in the cell population at the G0/G1 and S phases with 54.73% (from 55.05% to 24.92%) and 14.5% (from 34.18% to 29.22%), respectively. Moreover, marked augmentation was observed in the proportion of cells in the G2/M phase by 4.25-fold, and in the pre-G1 phase by 16.24-fold, in comparison to the control (DMSO). This clearly indicates that the target chalcone derivative 2c arrested the cell cycle proliferation of MCF-7 cells in the G2/M phase.
Design, synthesis, anticancer evaluation, and molecular modelling studies of novel tolmetin derivatives as potential VEGFR-2 inhibitors and apoptosis inducers
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2021
Asmaa E. Kassab, Ehab M. Gedawy, Mohammed I. A. Hamed, Ahmed S. Doghish, Rasha A. Hassan
Anticancer agents exert their cytotoxic action by aborting cellular proliferation at certain checkpoints. These checkpoints are distinguishable phases in the cell cycle, whose suppression results in the termination of the cell proliferation. Cell cycle analysis employs flow cytometry to distinguish cells within the different cell cycle phases. In this work, the effect of the most potent compound 5b on the cell cycle progression was scrutinised in order to explore the definite phase at which cell cycle arrest takes place in the HCT-15 colon cancer cell line. HCT-15 cells were treated with IC50 concentrations (6.62 µM) of compound 5b and its effect on the cell population in different cell phases was recorded and displayed in Table 3 and Figure 5. Interestingly, exposure of HCT-15 cells to compound 5b resulted in significant decline in the cell population at the S and G2/M phases with 16.88 and 65.61%, respectively. Moreover, marked augmentation in the proportion of cells in the G0-G1 phase by 1.32-fold, and in the Sub-G1 phase by 18.7-fold, in comparison to the control (DMSO). This indicates that the target tolmetin derivative 5b arrested the cell cycle proliferation of HCT-15 cells in the G0-G1 phase.
Induction of different cellular arrest and molecular responses in low EGFR expressing A549 and high EGFR expressing A431 tumor cells treated with various doses of 177Lu-Nimotuzumab
Published in International Journal of Radiation Biology, 2020
ShishuKant Suman, Rashmi Priya, Mythili Kameswaran
In response to DNA damage, cell-cycle progression and cell arrest were analyzed. Cell-cycle analysis is based on the quantitation of different amounts of DNA present at various stages of the cell cycle, which can be detected by DNA-binding dye in fixed cells and acquired on a flow cytometer. As per Guava cell-cycle reagent kit protocol, the cell-cycle progression was analyzed at 24 h post-treatment, in A431 and A549 cells which were untreated and those which were treated with 3.7 MBq, 18.5 MBq, and 37 MBq of 177Lu-Nimotuzumab. Briefly, ∼1 × 105cells (untreated and treated cells) were washed with PBS (0.05 M, pH7.4) and fixed in 70% ice-cold ethanol. The cells were kept at 4 °C for minimum 1 h, prior to staining. For staining, ethanol was completely removed from the cell suspension by repeated washes with PBS (0.05 M, pH 7.4). The cells were suspended in 200 μL Guava cell-cycle reagent and incubated at RT for 30 min in dark. Sample data were acquired using the Cell Cycle software module in Guava EasyCyte Flow cytometer and analyzed using Cyflogic software. The percent of cells at different stages of cell cycle was compared between the untreated A431 and A549 cells and cells treated with 3.7 MBq, 18.5 MBq, and 37 MBq of 177Lu-Nimotuzumab, to determine the cell-cycle arrest.